Hepatic encephalopathy clinical performance

HE patients with clinical manifestations, the original liver disease due to the type, the extent of the damage liver cells and different incentives and different. Have their clinical symptoms, clinical and laboratory examinations, and other types were described below.

(1) clinical symptom

HE the clinical symptoms, mainly mental, neurological abnormalities both.

1. Mental disorders

(1) disturbance of consciousness: Early manifestations of insomnia or circadian sleep upside down; While a further lethargy in the outside world unresponsive; More emphasis is manifested as drowsiness, or mental disorder; Finally in a coma, on the outside world is no response.

(2) smart change: Early simple counting retardation, attention is not focused; Further, a simple counting errors, things of the past memory loss, the unclear concept of space-time (time / disorientation); More emphasis on the figures when the concept of fuzzy, self-final loss (loss of self ), not statements for the performance of their own names, ages, occupations and so on.

(3) changes in personality and behavior

Personality changes: Early performance as difficult to detect depression or euphoric, rap message; Further, exciting, emotional, or anxiety, apathy; More emphasis on the performance of fidgety or manic.

Behavioral change: Early performance for the normal behavior of exaggeration, such as graffiti, litter, spitting fouling, spitting; Further, abnormal behavior, such as clothing touch bed and find other unconscious movements movements; More emphasis on the performance of persecution paranoia or paranoid.

2. That is abnormal nerve neuromuscular movement disorders, early performance metabolic tremor (metabolic tremor) such as jitter, or Flapping-Wing-like tremor, muscle action uncoordinated, writing chaos, but normal reflex exist, pathological reflex negative (-); Further Visibility Flapping-Wing-like tremor or add jitter, Language intermittent unclear, ataxia, or the lower normal reflex hyperparathyroidism, pathological reflex (+), muscle tension can be increased. while a heavier nystagmus, muscle tension has noticeably increased, or tonic clonic; eventually normal and pathological reflex disappeared, the pupil to expand, Kok arch anti-Zhang.

3. Apart from these other clinical manifestations, but also from HE patients breath sniff out a characteristic odor, which some describe as Anabaena odor smell, smells rotten apples, eggs degenerate garlic-like odor or smell, and so on. This is the smell of blood mercaptan content due to increased emission of breath.

Often patients with advanced HE appeared excessive ventilation (hyperventilation), often secondary to hypokalemia, acidosis and cerebral edema, and other complications; Blood NH3 can stimulate the respiratory center, the ventilation induced by excessive Pai NH3.

(2) clinical types (HE classification details)

According to the symptoms of modern whether HE, HE will be divided into two kinds: ① symptomatic HE: according to the degree of severity of symptoms I - IV class; ② minor HE: no clinical symptoms, but IQ, evoked potential testing anomalies. HE-and C-type three subtypes:

1. Attack of acute HE HE equivalent past, but does not include the type A HE attack, and some patients have some incentive (of incentives) and others as spontaneous type (without incentives type), was repeatedly attack (recurrence type); After the active treatment fully restored to normal mental state base Line level (0), each attack cycle days, two adjacent attack cycle between irregular intervals.

2. Persistent chronic HE HE equivalent past, his mental state in a sustained abnormal baseline (I level), can not be restored to normal baseline levels, based on this cropped up again, aggravated sexual attack, a week of each cycle of attack, the difference in time interval. HE Ⅰ for the light - and heavy as HE Ⅱ - Ⅳ.

3. HE that is of minor stressing subclinical HE, HE This is the occult, such patients without clinical manifestation, or detected only in IQ evoked potentials were found when the inspection; Or use special detection method can be found abnormal brain metabolism. Minor HE portal hypertension in patients with liver cirrhosis in the detection rate is as high as 60% -70%.

Brain degeneration of the liver, can be regarded as continuing HE, the CNS often exposed to the toxic metabolites of the role, from the brain tissue degeneration, with the exception of astrocytes, neurons may have a broad disappeared, a cavernous changes were seen mainly in gray areas to basal ganglia involvement more obvious. Some such performance in patients with irreversible mental, neurological symptoms, hand, foot-moving, action inflexible, and the EC ataxia, and other extrapyramidal symptoms, and because of the degenerative brain tissue, it said liver brain degeneration , liver or brain degeneration was to show different from Wilson’s disease. HE continuing to rely on long-term drug treatment (treatment-dependent).

(C) laboratory

1. Biochemistry

(1) Liver function tests: To understand the extent of liver damage, liver functional reserve, as well as the severity of illness and prognosis. Including: ① serum bilirubin; ② serum total protein, albumin, globulin; ③ serum enzymes: ALT, AST, AKP, GGT; ④ serum total cholesterol and cholesteryl ester; ⑤ prothrombin time / activity.

(2) blood urea nitrogen, creatinine, electrolytes, and other checks.

(3) Blood NH3 check: blood ammonia levels are usually higher than the blood ammonia content, and distributed evenly stable than the latter, the brain metabolism of ammonia mainly from blood, blood ammonia levels and brain uptake of NH3 in a linear correlation, and the grading and HE was significantly correlated, The blood ammonia content is not.

(4) Plasma amino acid check: check blood BCAA content and AAA, and AAA BCAA to understand the ratio normal BCAA / AAAthan> 3, HE ratio <1.

2. Electrophysiological examination

(1) electroencephalogram (EEG): HE have some prognostic value, but no specific diagnosis HE because metabolic encephalopathy similar changes can be, it only suggested that EEG changes in brain function. Normal people, the EEG amplitude low frequency (cycles per second amplitude cycles per second; Cps) faster, HE, with the condition progress gradually increased amplitude, and frequency gradually slow down. Q-wave coma for early and late in δ wave.

(2) evoked potentials (evoked potential): electricity to stimulate the potential to induce changes in the brain, and compared with the normal, the diagnosis of minor significance HE reference to a certain extent.

Visual evoked potentials (visual evoked potential; VEP): Determination of brain-stimulating visual occipital cortex of the brain caused potential changes. Now that the minor HE VEP diagnostic sensitivity is not high, individual differences of greater vulnerability to the impact of patients with psychological conditions.

Auditory Evoked Potentials (auditory evoked potential; AEP): The computer control the voice sound stimulation to induce CNS potential. The diagnostic evaluation of the significance of minor HE different VEP generally considered more sensitive.

Somatosensory evoked potentials (somotosensory evoked potential; SEP): median nerve stimulation to the cortex evoked potential changes in the value actually used to be further verified.

3. Intelligent Test, also known as psychological test (psychometric test), the most simple and easy to connect to digital test (NCT), can be divided into A and B two, NCT-A marker will have 1-25 decentralized digital box sequence by 1, 2, 3 … linking NCT — B is labeled with 1-13 and the letters A-L’s box, according to 1A, 2B, 3C … link up the order. Both NCT-A or NCT-B, Normal dollars divided into 15-30 seconds, the points classification extension and was positively correlated HE, HE can be early detection of minor patients. The test by education level, age and the learning effects.

4. Imaging examination imaging examination main magnetic resonance imaging (magnetic resonance imagine; MRI) and proton magnetic resonance spectroscopy of (proton magnetic resonance spectroscopy; MRS), in patients with liver disease to observe the changes in brain metabolism. Geisslep such as MRS and MRI detected by histology confirmed cirrhotic patients 51 cases of cerebral metabolism, and 36 cases of healthy people as controls. MRS show: cirrhotic patients in the white matter and gray matter inositol / creatinine (myoinosital / creatine) and choline / creatinine (Choline / creatine) the ratio of the two, than the control group were significantly lower (P <0.0001), and glutamine / glutamate (glutamine / glutamate ) is the ratio compared with the control group were significantly higher (P <0.0001); MRI clearly showed that the basal ganglia in high-density signal. The cerebral metabolic abnormalities can be seen in the minor HE not the patients with liver cirrhosis. Author think MRS, MRI may be even earlier, the objective to discover that the brain metabolism in patients with liver cirrhosis abnormal. This minor HE the early diagnosis can provide some clues.

The pathogenesis of hepatic encephalopathy mechanism

The understanding of the pathogenesis of HE, has experienced than half a century. As early as the 1950s, McDermott and Adams (1954) for the first time established the ammonia poisoning theory, since laid a milestone in the pathogenesis of HE. In the 1960s Zieve nerve in a variety of toxic substances (NH3, mercaptan, fatty acids, etc.) by HE synergy studies, and made a variety of neurotoxins synergies hypothesis (multiple synergistic neurotoxin hypothesis). In 1971 Fischer and established a false Balderassini neurotransmitter theory, and then developed into Murno, and other amino acids in plasma insulin imbalance doctrine, James (1979), will blood NH3, plasma amino acids and amino acid imbalance in blood - brain transit between the united as one, a door of the unified theory encephalopathy (uuified theory), 1982 Schafer and Jones also revealed γ-aminobutyric acid (gamma-a-mino - butyric acid; GAGB) in the pathogenesis of HE the role of this theory with ammonia poisoning and the importance of the same doctrine, that HE is still a new concept of the pathogenesis. 1985 Bengtsson on tryptophan-mediated changes in the neural chemicals role in the pathogenesis of HE. In 1995, Yurdaydin with sulfur acetamide (thioacetamide) AHF induced animal model of blood brain opioid peptide (opioid peptides) changes, such that the incidence HE peptide is one of the factors, and could use its antagonist for treatment. Moreover, in the pathogenesis of HE, in recent years scholars have attached particular importance to the toxic metabolite astrocytoma cells. In short, as the development of the times, mankind’s understanding of the pathogenesis of HE are constantly deepening appearance between the theory is independent of each other, but in fact from different sides expounded the pathogenesis of HE, are complementary to each other; Modern think ammonia poisoning in the pathogenesis of HE play a central role, GABA from synergies.

(1) Ammonia poisoning theory

So far ammonia poisoning theory still regarded as the classic doctrine HE incidence. The basis for the support of this theory: ① HE patients often Hyperammonemia; ② evoked some incentives HE often caused Hyperammonemia; ③ Clinical and Experimental Research shows that: induction Hyperammonemia HE and the occurrence of a certain relevance; ④ lower Hyperammonemia measures can effectively improve or alleviate the HE Attack. The pathogenesis of ammonia poisoning include NH3 sources, production, increased absorption and / or removal reduction, as well as ammonia toxicity.

1. The source of ammonia production, increased absorption

(1) increase the sources of ammonia: Exogenous NH3 major nitrogenous material from the gut, such as gastrointestinal hemorrhage, high-protein diet, and azotemia the intestinal hepatic urea cycle. Secondly delinking from the amino role in generating NH3 in negative nitrogen balance, muscle wasting and severe infection such circumstances, endogenous NH3 increase.

(2) ammonia production increase: nitrogenous substances in the right colon bacteria generally under-Generation NH3, in patients with liver disease due to bacteria and reproductive disorders Cong strong secretion of urease enzyme and amino acid oxidation increase, resulting in the small intestine and colon-NH3 increase; In recent years scholars, portal hypertensive gastropathy, , Helicobacter pylori can cause ammonia production increase.

(3) increase the absorption of ammonia: Under normal circumstances, the content within the lumen of pH <6:00, even the generation of large amounts of NH3, but most of the ammonium form (NH4 +) with feces from in vitro; Severe liver disease hypokalemia, low chlor-alkali poisoning, intestinal pH> 6 , generated NH3 substantial absorption into the systemic circulation, cause Hyperammonemia.

Based on the foregoing, NH3 sources decided to gut the contents of the substances in nitrogen, ammonia production decision on the role of bacterial enzymes, ammonia absorption in the intestines decision of pH, the three links of this treatment guide HE still practical significance.

2. Ammonia removal of the material reduction in nitrogen metabolism, mainly through amino acid oxidation from Amino (- NH2) reaction of NH3. The liver is the most important in vivo metabolism of nitrogen organ, followed by the brain, muscle and kidney, these organs on the one hand through oxidation from the amino role Generation NH3, on the other hand, through the urea cycle and / or alpha-ketoglutarate - glutamic acid - glutamine way to continuously remove NH3 to peacekeeping a blood NH3 the dynamic balance. Hepatic blood NH3 dynamic balance in the maintenance plays a very important role. Severe liver disease mainly in the liver remove NH3 dysfunction, followed by the kidneys and muscle.

(1) removal of NH3 role in the liver decreased: the door of the surrounding area within the liver cells are rich in mitochondria enzyme glutamine (glutaminase) it will catalyze glutamine formation glutamate with NH3.

The liver cells themselves generate NH3, and from the portal blood NH3 (Gut), as well as from the hepatic artery blood NH3 (endogenous) are both in liver cells via two metabolic pathways clearance, serious liver disease, the following two ways metabolic clearance decreased, resulting in Hyperammonemia.

Ornithine cycle (urea cycle) channels

Ornithine cycle, also known as urea cycle, in NH3 metabolic clearance is the most important way, but also of liver-specific nitrogen metabolism functions, but not other organs. Ornithine cycle with the above-mentioned liver cells NH3 formation is the interface between, also at the door area surrounding liver mitochondria, the area is rich in mitochondria - carbamoyl phosphate synthase (carbamyl phasphate synthetase; CPS) and ornithine amino formyl transfer enzyme (ornithine carbamyl transferase; OCT), CPS catalytic ammonia synthesis of amino carbamoyl phosphate, while catalytic OCT ornithine amino carbamoyl phosphate and the amino-cresol to form citrullinated (citrulline), which is the initial stage of urea cycle is the most important step. Severe liver disease, OCT CPS and vitality obvious damage, mitochondrial uptake NH3 capacity reduced ATP production and reserves are insufficient, ornithine cycle lack of energy supply. These factors seriously affect ornithine cycle, and hinder NH3 use of urea synthesis, resulting Hyperammonemia.

Α - ketoglutarate - glutamic acid - glutamine metabolism pathway

This metabolic pathway and the urea cycle remove NH3 role, compared to only lies in second position; In addition to liver, muscle, brain and have such a function. Central venous Hepatic Lobules around the liver cells, for this is the main place metabolism, liver cells in the area only if it is involved in the metabolic pathway of the enzyme system that glutamate dehydrogenase (glutamic dehydrogenase; GLDH) and glutamine synthetase (glutamine synthetase; GLS), GLDH catalytic ammonia and α - ketoglutarate combination of glutamic acid, urea cycle in the NH3 in the circumstances, this reaction was reversible reaction steps (using dotted line reactive said); GLS, and NH3 with catalytic glutamate generated glutamine.

When serious liver disease, GLDH activity and GLS also severely damaged liver metabolic pathway through the removal of NH3 role also diminish.

(2) renal excretion NH3 role damage: the organ through α - ketoglutarate - glutamic acid - glutamine way to the formation of glutamine, the release cycle to the system and re-exported to renal distal convoluted tubule cells, catalytic glutamine enzyme and GLDH, from generation NH3 with the amino price anion α - ketoglutarate (α - KG2-), In addition, renal cell within the carbonic anhydrase (CA) carbonate formed by carbon dioxide, which dissociation of hydrogen ions H + and HCO3-, renal distal convoluted tubule cells generated through the metabolic process of NH3 and H + secretion together tubular cavity to form ammonium salt, with the urinary excretion, the Health 10% of HCO3-to re-absorb the blood circulation, so as to effectively conditioning cycle of acid-base balance.

Patients with severe liver disease, such as with renal dysfunction or low potassium, low chlor-alkali poisoning, and the formation of H + secretion reduction, NH3 it is difficult to form NH4 + excretion by renal tubular cells, re-absorbed into the systemic circulation.

Lockwood with markings such as nitrogen (13 N) of ammonium chloride (13 NH4C1) intravenous injection, and minutes later observed 13 NH3 in vivo distribution, muscle use 13 NH3 or injection of about 50%, and in the form of glutamine, brain accounts for about 7% to 8%, liver or about 7 %, This muscle is also NH3 metabolism suggested that an important place. Patients with severe liver disease, muscle wasting, and its use of NH3 role correspondingly weakened.

3. The toxicity of ammonia

(1) reduce the CNS in Na +-K +-ATPase activity: ammonia and other toxic metabolites such as mercaptan, phenol, short-chain fatty acids, which are synergistic toxicity of BBB and can directly damage the nerve cell membrane Na +-K +-ATPase activity. BBB activity decreased, the BBB weakened role of barriers, some under normal circumstances be toxic enzyme decomposition products such as GA-BA can not stop access to CNS, caused HE. Cranial nerve cells and astrocytes of the membrane Na +-K +-ATPase has a high vigor, in order to maintain CNS excitatory ion conduction gradient, NH3 through competitive inhibition of K + and Na +-K +-ATPase activity, not only can cause nerve impulse conduction obstacles , and can cause edema astrocytes or cerebral edema.

(2) interfere with the energy metabolism of CNS: Under normal circumstances, glucose enter the CNS through the BBB, is dependent on its enzyme system destined for the poor against the concentration of CNS, the BBB functional impairment, poor concentration of glucose transporter inverse reduction; In addition, high-NH3 hyperlipidemia, NH3 through α-keto glutaric acid - glutamic acid - glutamine metabolism means, consume a large amount of alpha-ketoglutarate; CNS respectively over the impact energy supply and jamming its energy metabolism.

(3) can interfere with glutamate neurotransmitters (glutamateric neurotransmission): CNS is the glutamate excitatory neurotransmitter, and most widely distributed brain is a neurotransmitter. Under normal circumstances, glutamate synapses (glutamateric synapse) nerve impulse conduction, through glutamate - glutamine cycle to adjustments. NH3 from BBB to enter the CNS, the first uptake by astrocytes in its glutamine synthetase catalyst, generating glutamine, which entered the part of presynaptic neurons, and the other part into the cerebrospinal fluid (CSF). Presynaptic neurons of glutamine, in its role of glutamine, glutamate production, storage and release in vesicles within the synaptic gap to, and part of postsynaptic neurons glutamate receptor binding, it can start the neurotransmitter glutamate, the other part from astrocytoma reuptake, weight a new beginning another round of glutamate - glutamine cycle. Hyperammonemia, astrocytoma cells glutamate and NH3 with a large number was reduced consumption, generating a corresponding glutamine increased significantly; Former synaptic neurons glutamine due to the activity of glutamine by ammonia toxicity of weakened, we can not generate glutamate, thereby blocking the normal glutamate — glutamine cycle, can interfere with the neurotransmitter glutamate. Modern research also shows that: cell Glutamyl content too high, can cause cytotoxicity brain edema.

(4) interference with nerve action potential (nerve action potentials): NH3 enable neurons chloride off pump (neuronal chloride extrusion pump) inactivated so that the neuron depolarization, the inhibition of excitatory postsynaptic potentials in the formation and inhibit axon conduction (axonal conduction).

It must be pointed out: Hyperammonemia not necessarily caused HE, HE incidence is not the only factors or the deciding factor. Blood NH3 mainly come from the gut, but intestinal addition NH3, there are other toxic metabolites (such as GABA, etc.), can also cause HE; HE some incentives, encouraging high NH3 hyperlipidemia, can also lead to other toxic product cycle accumulation in the system; Lowering blood NH3 measures, they the same can reduce other toxic content in the blood; Therefore, we can not simply HE incentive to drop NH3 measures and the support of ammonia poisoning as the basis for the theory. But from another point of view, Hyperammonemia and other poisons by HE synergies, so far has drawn wide attention.

(B) gamma-aminobutyric acid theory

Γ-aminobutyric acid (GABA) CNS is the most important inhibitory neurotransmitter, distributed in almost all parts of the brain. Under normal circumstances, blood circulation in the GABA transporter to BBB, its enzyme system by delinking amino acid production and deactivation, it can not enter the brain through the BBB, the brain GABA in the presynaptic neurons generated, or glutamic acid in the enzyme from hydroxyl (GAD) a catalyst, generating GABA from hydroxy, and stored in the vesicles, it has no biological activity at this time, to be released after the synaptic gap, and the postsynaptic membrane surface of neurons Supramolecular receptor complexes (supermolecular receptor complex) combination can only show its inhibitory neurotransmitter GABA role. The so-called Supramolecular receptor complexes by GABA, benzodiazepine (benzodiazepine; BZ), Barbiturates (BARB), and other receptors, as well as chloride ion (Cl-) channel composed of tight junctions, when GABA and complex combination, chloride channel open, C1-enter neurons , membrane potential caused hyperpolarized (membrane hyperpolarization), which is GABAergic inhibitory neurotransmitter conduction foundation. Given the complex formed by three receptor, the receptor ligand three have coordinated non-competitive sites, it BZ receptor agonist agents (such as stability) and BARB drugs can enhance the biological effects of GABA.

Severe liver disease, CNS GABA mainly come from the gut, it is in the intestinal bacterial enzyme produced under The portosystemic shunt, or liver for the first time, without a role to enter the system through the cycle, in the BBB enzyme system activity reduced circumstances, the GABA unstoppable enter the brain and CNS neurons and the membrane Supramolecular receptor complex combination of inhibitory neurotransmitters play its biological effects, resulting in HF. The results show that: HE patients with CNS neuronal membrane receptor on the supramolecular complexes density and affinity of the receptor was increased several times; Application receptor antagonist including B7 the antagonist fluoride Mazzeni (Flumazenil; R015 - 1788), can significantly improve the clinical performance of HE. The above theory suggested that GABA neurotransmitters in the pathogenesis of HE, is of great significance.

(C) endogenous benzodiazepine Hypothesis

Benzodiazepine (benzodiazepines; BZ) Supramolecular receptor is a part of receptor complexes, HE patients and experimental animal model of liver failure, blood brain endogenous BZ-like substances are increased, which suggested that endogenous BZ-like substance with the same combination of complex HE caused, at least in part to strengthen inhibitory GABA nerve conduction. NH3 with natural BZ receptor ligand interactions, or endogenous BZ analogues have synergies, directly enhance GABAergic neurotransmitters, to contain CNS function.

(D) endogenous opioid peptides

HE recently found in patients with central nervous system opioid receptor expression and serum levels of endogenous opioid peptides increased application of its antagonist resume consciousness, so that it in the pathogenesis of HE play catalytic role.

(5) false neurotransmitter / amino acid imbalance theory

1. False doctrine food neurotransmitter in aromatic amino acids (AAA) in the case of phenylalanine and tyrosine, the intestinal bacteria decarboxylase, respectively tyramine and phenylethylamine generation, both amine from intestinal absorption, under normal circumstances in intrahepatic decomposition clearance, serious liver disease or portosystemic shunt, not liver metabolism systemic clearance to enter, and the transit system through the BBB to enter the brain, the role of non-specific hydroxylase, respectively, and the formation of hydroxyl Phenylethanolamine Phenylethanolamine / Chapter Amine, the chemical structure of the two with normal neurotransmitter norepinephrine (really transmitter) similar, but not really convey neural transmitters impulse role or roles weak, so called false neurotransmitter, when its uptake by nerve cells and nerve synapses in the accumulation to a certain extent, crowding out or replace normal really neurotransmitters, nerve impulse conduction occurred result, obstacles excited impulse not spread to cerebral cortex, the brain and thus inhibiting abnormal a disturbance of consciousness.

Pseudo neurotransmitter theory scholars so far have not been recognized, since the brain of laboratory animals injected massive number of false indoor transmitter, and do not raise their awareness of obstacles, died of cirrhosis in patients with HE, false neurotransmitters in the brain but does not increase the lower level does not really reduce transmitter instead increase production of neurotransmitters increase really drugs such as levodopa, bromine implicit stop, there is a lack of therapeutic effect. The current theory is that this does not have any clinical significance.

2.

BCAA with Valeriana-, amino-, iso-leucine three, which under normal circumstances is not the liver metabolism, absorption after portal vein directly into the system cycle, and was skeletal muscle, cardiac muscle, brain and other organs organizations uptake metabolism, as a part of their energy supply. Severe liver disease, an increase in plasma insulin levels, prompted BCAA in these organ tissue uptake metabolism strengthened, resulting in reduced serum BCAA.

AAA benzene phenylalanine, tyrosine and tryptophan, a serious liver disease when their blood content increase, and because of BCAA reduce blood levels, AAA BBB transit system competitive advantage over BCAA entering the brain, phenylalanine, tyrosine a false neurotransmitters, leading to HE; Tryptophan enter the CNS, metabolism of 5 - serotonin, which is a inhibitory neurotransmitter in the accumulation of vesicles within certain extent, it can cause unconsciousness.

Plasma amino acid imbalance theory main theory is based on the false transmitters, as the latter in the role of the pathogenesis of HE has been criticized, and this has shaken the amino acid imbalance theory in the pathogenesis of HE status.

(6) other toxic substances

1. Mercaptan sulfur amino acids (methionine, cystine) in the intestinal delinking from amino and carboxyl Generation methyl mercaptan (HS-CH3), Ethanethiol (HS-CH2CH3) and dimethyl sulfide (H3C-S-CH3), normal metabolism in the liver was serious liver disease with their blood volume increased, affecting the integrity of BBB, and synergies with the NH3 have toxic effects.

2. Short-chain fatty acids means eight carbon atoms less fatty acids, a serious liver disease, peripheral adipose tissue using increased blood from the liver can be used intake, the content of blood increased, when his transfer to CNS, hinder brain tissue oxidative phosphorylation coupling, disrupted brain energy metabolism, video ring for the nerve cell membrane and the effects of the neurotransmitter synaptic transmission parts, and NH3 are synergistic toxicity.

3. Manganese (manganese) excretion by the liver, cirrhotic patients with elevated manganese content. MRI proved: the brain in patients with liver cirrhosis globus pallidus (globus pallidus), a manganese deposits, which showed that high-density, and integration with extrapyramidal symptoms correlated, but the stage has nothing to do with HE. HE manganese poisoning in the pathogenesis of the role proved to be more information.

Hepatorenal syndrome

Severe liver disease, often with renal hemodynamic changes and renal dysfunction, clinical performance for the lower creatinine clearance rate <40 ml / min, the serum creatinine> 133 μ mol / L, dilution of hyponatremia (<130 mmol / L), oliguria (<500 ml / d) or no urine ( <100 ml / d), for hepatorenal syndrome (hepatorenal syndrome; HRS); due to the lack of anatomic or pathologic evidence of change, it is also called functional renal failure (functional renal failure; FRF).

The treatment of hepatic encephalopathy

Hepatic encephalopathy There is no magic therapy, treatment should take comprehensive measures:

(1) the elimination of incentives certain factors may induce or aggravate hepatic encephalopathy. Cirrhosis, the drug in vivo half-life extended dissection reduced the sensitivity of the brain in patients with encephalopathy increase, the majority can not tolerate anesthesia, analgesia, sedative-hypnotic, sedative and other drugs, such as improper use, there will be the drowsiness, until he lost consciousness. When patients with manic unrest or convulsion, banned morphine and its derivatives, vice aldehyde, Chloral Hydrate, pethidine and quick-impact Barbiturates may use CERs (constants, 1 / 2 or 1 / 3) stability, scopolamine, and to reduce delivery times. More non - Nai, chlorpheniramine, and other antihistamines sometimes medicine can be used for stability and maintenance. The importance of the timely control infection and upper gastrointestinal bleeding, avoid rapid and substantial Pai diuretic and potassium release ascites. To rectify water, electrolyte and acid-base balance disorders.

(B) reduce the generation and the intestines absorb poison

1. Starting a few days fasting diet protein. The daily supply of calories 1200 ~ 1600 kcal and adequate vitamins, carbohydrates as a main food, not eating can unconscious by nasogastric tube feeding. The fat can delay gastric emptying to use less. Nasal feeding on the best use 25% of sucrose or glucose solution per ml of 1 kcal production, daily into 3 to 6 g essential amino acids. Gastric emptying should not stop nasal feeding, and deep vein catheterization using drip 25% glucose solution to maintain nutrition. The massive infusion of glucose in the process, must be alert hypokalemia, heart failure and cerebral edema. He was clearly, it can gradually increase the protein to 40 to 60 g / d. Different sources of protein induced coma different from the trend is generally believed that meat protein induced encephalopathy biggest role, followed by milk protein, plant protein minimum, it corrected the negative nitrogen balance patients to use vegetable protein for the best. Plant protein containing methionine, less aromatic amino acids, branched-chain amino acids containing more, and can increase fecal nitrogen excretion. In addition, the plant protein containing non-absorbable fibers, glycolysis by intestinal bacteria acid production to the exclusion of ammonia, and the favorable purge, it applies to patients with hepatic encephalopathy.

2. Enema plot or catharsis removal of enteral feeding, blood or other nitrogen-containing substances can be used saline or weak acid solution (for example, dilute acetic acid solution) enema, or oral or nasal feeding 25% magnesium sulfate 30 ~ 60 ml catharsis. Acute portosystemic shunt in patients with encephalopathy coma with lactulose 500 ml water 500 ml enema as a first treatment, particularly useful.

3. Inhibit bacterial growth oral neomycin 2 to 4 g / day or election-serving Palestinian adriamycin, kanamycin and ampicillin have good effect. Neomycin’s long service in a small number of patients with renal function in the hearing or derogation, it should not take more than a month neomycin. Oral metronidazole 0.2 g four times daily, efficacy and neomycin same applies to those renal dysfunction.

Lactulose (lactulose, β - galactosidofructose) after oral bacteria in the colon which has been split into a lactic acid and acetic acid, mesocaval was acidic, thereby reducing ammonia formation and absorption. abdominal cramps, nausea, vomiting, and so on. In recent years found that the lack of lactase lactose in the colon in the crowd, acid production by bacterial fermentation stool after lower pH, reduce ammonia content, for the treatment of hepatic encephalopathy, and the effect of lactulose, and cheaper.

(C) to promote the metabolism of the elimination of toxic substances, correct amino acid metabolism disorder

1. ① down ammonia drug potassium glutamate (each 6.3 g/20ml, potassium content 34 mmol) and sodium glutamate (each 5.75 g/20ml, Sodium 34 mmol), each with four by adding glucose solution intravenously daily 1-2 times. Glutamate potassium, sodium, as the proportion of serum potassium, , and edema, ascites obviously cautiously uses sodium agent. ② arginine 10 ~ 20 g glucose solution by adding a daily infusion, the drug may call a dynamic synthesis of urea, the drug was acidic, apply to patients with high blood pH. Descending ammonia drugs on the chronic recurrent portosystemic shunt encephalopathy better efficacy of severe hepatitis-induced acute liver coma invalid. ③ sodium benzoate with enteral residual nitrogen quality such as glutamine or glycine to form hippuric acid, from the kidney, thus lowering blood ammonia. Treatment of acute encephalopathy portosystemic shunt and the effect of lactulose considerable. The second daily dose, oral 5 g each. ④ phenylacetate and enteral glutamine to form non-toxic hippuric acid excretion by the kidneys, can lower blood ammonia concentration. ⑤ ornithine - α - ketoglutarate and ornithine aspartate drop markedly over the role of ammonia.

2. Branched - chain amino acids of oral or intravenous infusion in branched-chain amino acid-based amino acid mixture, in theory, can help redress the imbalance of amino acid metabolism, inhibiting neurotransmitter in the brain leave the formation, but the portal shunt encephalopathy effect still controversial. Branched - chain amino acids than the average consumption of protein induced coma smaller role, if patients can not tolerate protein food, adequate intake of the rich in branched-chain amino acid mixture with the resumption of the positive nitrogen balance is effective and safe.

3. GABA / BZ receptor antagonist compound GABA receptor antagonist bicuculline have (bicuculline), , and 78% of patients with cirrhosis and somatic symptoms evoked potential (SEP) has noticeably improved, but a few hours after the withdrawal symptoms of relapse. such as three minutes after the EEG without improvement, increased to 0.4 mg dose, and then 0.8 mg, 1 to 2 mg, the largest one case of a total dose of 9.6 mg, 14 patients with 71% improvement. I use the hospital dose of 0.5 mg and 0.9% normal saline 10 ml in five minutes after injection, and then 1.0 mg 250 ml of normal saline drip 30 minutes, the liver cirrhosis associated with the symptoms of encephalopathy in a great improvement.

(4) liver transplantation for many There is no other satisfactory method of treatment can reverse the chronic liver disease, liver transplantation is a recognized effective treatment. Because of the transplant operation process improvement and standardization of methods and preservation of donor liver surgery and technological advancements, in patients after transplantation has been greatly increased the survival rate (see Chapter liver transplantation).

(5) Other symptomatic treatment

1. Corrected water, electrolyte and acid-base balance disorders to the total daily income of no more than 2500 ml suitable. The entry in cirrhotic patients with ascites fluid volume should increase control (generally about urine output increases 1000 ml), so as not to dilute the blood, hyponatremia are too small to add a coma. And promptly correct potassium deficiency and alkali poisoning, potassium deficiency who added potassium chloride; Alkalosis arginine salt solution are available intravenous drip.

2. To protect brain cells function intracranial lower temperature with ice cap, in order to reduce energy consumption and protect brain cells function.

3. Maintain airway patency deep coma, should be tracheotomy reoxygenation.

4. Intravenous infusion of cerebral edema hypertonic glucose, mannitol and other dehydrating agent to combat brain edema.

5. To prevent bleeding and shock, bleeding tendency, vitamin K1 or intravenous drip blood transfusion to correct shock, hypoxia of uremia and renal ago.

6. Peritoneal dialysis or renal azotemia such as hepatic encephalopathy is the reason, peritoneal or hemodialysis may be useful.

Treatment of chronic cholecystitis

Lack of chronic cholecystitis often obvious symptoms, decreased appetite frequently manifests itself, upper abdominal bulging nausea, discomfort and the navel, therefore, people often mistakenly considered to be “a stomach illness.” There are also some patients suffering from acute cholecystitis, he was missed or misdiagnosed and eventually developed chronic.

The treatment of chronic cholecystitis and anti-inflammatory mainly Lidan mainly used Lidan drugs may choose to use:

(1) Oral 50% magnesium sulfate solution, each 10 ml, three times a day;

(2) sodium cholate, oral each 0.2 grams daily 3 to 4 times;

(3) dehydrogenase acid is a Lidan drug tablets, oral each 0.25 mg three times daily;

(4) Shudan Qualcomm, oral each 40 mg three times daily.

These drugs can be optional under the guidance of a doctor or the combined use of two kinds of conduct. If inflammation may increase with penicillin, but they must do so after injection skin test administration, you can also use cephalosporin antibiotics, but also oral ciprofloxacin tablets, each 0.25 grams, three times per day. Chinese medicine Xiaoyanlidan films have anti-inflammatory and choleretic at the same time, three times daily, every six, before eating clothes. Chronic disease is a chronic cholecystitis, the need for long-term medication, but because of the use of any drug efficacy will be reduced or can produce side effects, it can choose to turn some drug use.

Sometimes patients with chronic cholecystitis in abdominal pain, nausea, abdominal distension, etc., then the choice of metoclopramide, injection or oral administration pills can be. Each 10 mg intramuscular injection daily 2nd; Oral administration of 10 mg three times daily. Because chronic cholecystitis will cause indigestion, can take some medicine to help digestion, oral each two daily 3 to 4 times; Or yeast tablets, oral each 3 g three times a day.

Patients suffering from chronic cholecystitis should be low-fat diet, not to eat too much fat or fat foods (such as lard, pork, eggs, etc.), this would make her illness became more serious, the effects of the treatment.

Liver disease drug

Lamivudine 0.1g for therapeutic alliance Hepuding chronic HBV replication of liver
Andafen interferon a2b 300MU chronic hepatitis B and other viral diseases
A dry-subsidized complex above interferon 9mcg 18-year-old chronic HCV infection
The rivers and mountains ® thymosin 100mg cellular immune regulator
Famciclovir tablets 0.125g broad-spectrum antiviral HSV - I, VZV, HBV
Essentiale Capsule 300mg / tablets of fatty liver, liver cirrhosis, acute and chronic hepatitis
Tiopronin tablet tiopronin improve liver function and clinical symptoms
Ganlixin ALT injection with the chronic persistent hepatitis active hepatitis
Phyllanthus urinaria liver tablets 0.3g / Tablets
Of atomolan solvent 0.6g × 5 viral, liver damage due to drug toxicity
P transfer factor Liquid 100ml × 6 for immune dysfunction caused by various diseases
Astragalus injection 2ml × 10 of × 1 box
Fufang Danshen injection 2ml × 10 of × 1 box
Hepatitis B Ling 36g
Li Liver Pills 20g
Dongbao Zhigantai-1 × 48 × 100
Kushen-1 × 60
To pain tablets 2 × 1000
Hugan tablets 0.35g × 100 tablets
Fufang Danshen tablets 0.3g × 60 tablets
Jingguishenqi pill 9g × 10
Bi-liver capsule 0.3g × 2 plate × 12
Hugan Tablet 0.5g × 1 plate × 12
Lidan Pai flakes 100
Inosine injection 2ml 0.1g × 10 of
Inosine Liquid 20ml 0.2g × 10
Inosine - 0.2g × 100s
Ribavirin injection 1ml 100mg × 10
Ribavirin injection 10 × 1ml
Thymosin injection 2ml × 10
Hepatitis B detoxification capsules 0.25 × 12 × 2 plate × box Qingrejiedu Shuganlidan for hepatitis B

Adenosyl methionine

Adenosyl methionine in the human body is all organizations and body fluids of a molecular physiological activity, participation in important biochemical reactions. Help prevent intrahepatic cholestasis. For the treatment of liver cirrhosis before and after the intrahepatic cholestasis and intrahepatic cholestasis during pregnancy.

Dosage: initial treatment: daily 500-1,000 mg intramuscular or intravenous injection, a total of two weeks;

Maintenance treatment :1000-2000 mg / day, orally.

Specifications: 500 mg × 5, 500 × 10.

Glutathione

Glutathione is in the cytoplasm of human synthesis of a natural peptide, by Glutamyl, cysteine and glycine composition, containing sulfhydryl, there are important physiological functions. Through sulfhydryl are combined in vivo free radical can be easily transformed into the metabolism of acids substances, thereby speeding up the excretion of free radicals, protecting the liver synthesis, detoxification, inactivated hormones, and other functions, and promote acid metabolism, help digestive tract fat absorption and fat-soluble vitamins.

Dosage :300-600 mg / times a day 1-2 times, intramuscular injection or intravenous infusion.

Specifications: 300 mg / Extension, 600 mg / branch.

PHGF

PHGF from suckling pig liver is a small molecular weight peptide extracted active substances. The normal liver cells can be stimulated DNA synthesis, and promote liver regeneration, liver cell injury in a protective role in promoting the restoration of liver function. Also the body of the regulation of immune function and role of hepatic fibrosis. Clinic for the treatment of severe hepatitis, chronic active hepatitis and cirrhosis.

Dosage :80-120 mg / day, by adding 250 ml of intravenous solution.

Specifications: 20 mg × 10.

DDB China Liver Disease

DDB is rapid and effective JiangMei medicine can effectively reduce serum ALT level, but will rebound after stopping easy. In addition, the role of the drug on AST not obvious, some patients with chronic liver disease taking AST will arise after the increase.

Dosage: 7.5 mg, three times per day, restoring normal ALT should be gradual reductions.

Specifications: 1.5 mg × 250