A. Definisi In cholelithiasis, calculi (gallstones) usually form in the gallbladder from solid constituents of bile and vary greatly in size, shape, and. Asuhan Keperawatan Pada Pasien Dengan Gangguan Empedu: Batu to gallstones (cholelithiasis), more than 90% of patients with acute cholecystitis have. LAPORAN PENDAHULUAN ASUHAN KEPERAWATAN PADA KLIEN, Asuhan ASKEP LAPAROSCOPY CHOLELITHIASISmore. by Mae.
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Gallstone disease GD is a chronic recurrent hepatobiliary disease, the basis for which is the impaired metabolism of cholesterol, bilirubin and bile acids, which is characterized by the formation of gallstones in the hepatic bile duct, common bile duct, or gallbladder. GD is one of the most prevalent gastrointestinal diseases with a substantial burden to health care systems.
GD can result in serious outcomes, such as acute gallstone pancreatitis and gallbladder cancer. The epidemiology, pathogenesis and treatment of GD are discussed in this review.
Concept of the pathogenesis and treatment of cholelithiasis
The prevalence of GD varies widely by region. The prevalence of gallstone disease has increased in recent years. This is connected with a change in lifestyle: Ke;erawatan of the important benefits of early screening for gallstone disease is that ultrasonography can detect asymptomatic cases, which results in early treatment and the prevention of serious outcomes.
The pathogenesis of GD is suggested to be multifactorial and probably develops from complex interactions between many genetic and environmental factors.
Asuhan Keperawatan Cholelithiasis
It keperaeatan that corticosteroids and oral contraceptives, which contain hormones related to steroid hormones, may be regarded as a model system of cholelithiasis development in man. The achievement in the study of the physiology of bile formation and the pathogenesis of GD has allowed expanding indications for therapeutic treatment of GD. Gallstone disease GD cholelithiasis is one of the most prevalent gastrointestinal diseases, with a substantial burden to health care systems[ 1 ].
Gallstones GS may form because of many different disorders[ 2 ]. GD is a chronic recurrent hepatobiliary disease, the basis for which is the impaired metabolism of cholesterol, bilirubin and bile acids, which is characterized by the formation of gallstones in the hepatic bile duct, common bile duct, or gallbladder[ 3 ].
Mae idasari –
GD and cardiovascular disease, common diseases worldwide, are strongly associated and have considerable economical impact[ 4 – 6 ]. GS are considered avoidable causes of death[ 9 ]. GD is a common disorder all over the world[ 10 ]. In Western countries, the prevalence of gallstone disease reportedly ranges from approximately 7. The prevalence of gallstone disease is also high in some ethnic groups, e. There is a steady-state trend for higher GD morbidity, which is associated with the improved diagnosis of the disease.
One of the important benefits of early screening for gallstone disease is that ultrasonography can detect asymptomatic cases, which results in early treatment and the prevention of serious outcomes[ 118 ]. The reference standard to detect GS was represented, not only by the ultrasonographic scan of the gallbladder, but also by the direct examination of the explanted liver[ 2 ]. The Hispanic and indigenous populations of the United States show particularly high morbidity rates[ 1920 ].
Epidemiological survey data in the United States suggest that approximately 20 million Americans suffer from GD.
At the same time, GD is, on the contrary, less characteristic for the peoples of southeast Asia, Africa and the far north[ 21 ]. The prevalence of gallbladder and biliary tract diseases among the digestive ones is GD is a multifactorial disease. In the general population, one of the main risk factors for developing GD is gender: Other factors are age, genes and race.
Additional factors are obesity, rapid weight loss, glucose intolerance, insulin resistance, high dietary glycemic load, alcohol use, diabetes mellitus, hypertriglyceridemia, drugs and pregnancy[ 2 ]. Four major groups of factors that contribute to the formation of cholesterol gallstones to some degree may be identified[ 2223 ]: Gallstone detection rates increase with age, which makes it possible to consider it one of the risk factors for GD[ 24 ].
No significant differences have been found in the frequency of gallstone formations in childhood and adolescence.
Cholelithiasis in children is an unusual finding but is not exceptional and is associated with nonspecific symptoms[ 2526 ]. After 20 years of age, the rate of gallstone hcolelithiasis increases with each decade[ 27 ].
The amount of cholesterol in the bile is supposed to increase with age[ 28 ]. PXR prevents cholesterol GD via its coordinated regulation of the biosynthesis and meperawatan of bile salts in the liver and intestine.
Cholesterol precipitation is prevented by increases in concentrations of biliary bile salts and a reduced cholesterol saturation index CSI [ 30 ]. Loss of PXR sensitized mice to lithogenic diet-induced cholesterol GD, characterized by decreases in biliary concentrations of bile salts and phospholipids and increases in the CSI and formation of cholesterol crystals. The reduced expression of CYP7A1 most likely resulted from activation of PXR and induction of fibroblast growth factor 15 in the intestine[ 30 ].
There is a negative correlation between age asuahn the amount of synthesized bile acids and a positive correlation between cholesterol levels and age. Furthermore, hemoperfusion of the gallbladder wall is noted to be reduced with age due to the presence of sclerotic changes.
This contributes to the dysfunction of the gallbladder, its infection and inflammation with exudation into the oeperawatan of the organ. The female gender is cholelithiasid generally recognized risk factor of GD[ 102431 – 33 ]. Marschall HU and Einarsson C[ 34 ] assume that age and sex are profoundly associated with the incidence of gallstone disease; the metabolic risk factors for gallstone disease are different between men and women[ 129 ]. In reproductive-aged women, the risk of cholelithiasis is times higher than that in men[ 10 ].
The reasons for this have not been fully elucidated. Keperawataan also contribute to formation of stones in the gallbladder[ 102233 ]. GD is particularly common in multiparas parity 4 or more.
Gender differences and asjhan GS detections in pregnant women are linked with hormonal background[ 10 ]. Elevated estrogen levels are known to increase cholelithiwsis excretion into the bile by causing its supersaturation with cholesterol. During pregnancy, in addition to the elevated level of estrogens, gallbladder evacuation function suffers, giving rise to bile sludge and gallstones.
Hormone replacement therapy HRT with estrogen-containing agents in postmenopausal women[ 35 ] and the use of hormonal oral contraceptives[ 19 ] may increase the risk of symptomatic GS. This confirms trial data and additionally shows effects of cholellthiasis of use and increased risk associated with past use[ 36 ].
Opinions regarding the association between gallbladder disease and oral contraceptives differ[ 19 ]. This may be associated with the fact that the effect of estrogens is dose-dependent. Therefore, the currently available low-dose estrogen-gestagen combination oral contraceptives have a lower risk for GD[ 10 ].
Regarding gender, despite of the higher absolute frequency of GS in females with cirrhosis, the risk of cholelithiasis in cirrhotic males is much higher than in the healthy population[ choleltihiasis ]. Fornari et al[ 37 ] claimed that cirrhosis is a risk factor for GD in males keperawaatn suggested that a high level of estrogens could play a role by an impairment of gallbladder emptying, as observed also in pregnant women. Age, sex and body mass index BMI keperawayan, relevant factors for GS development in the general population, are much less important in patients affected by cirrhosis where the main factor to be considered is the degree of impairment of underlying liver disease[ 2 ].
There keperawatwn growing evidence that GS formation may be keperawatna determined[ 38 ]. The risk of GS formation is times higher in individuals whose relatives suffer from GD[ 3239 ].
In cases of family GD, genetic factors play a prevailing role and are characterized by autosomal dominant inheritance[ 3140 ]. Genetic susceptibility contributes to the etiology of gallbladder diseases, as shown by multiple epidemiological studies. Murine experiments have shown that there is a lithogenicity gene[ 41 ]. A major gallstone susceptibility locus Lith6 was identified in by quantitative trait locus mapping in mice.
Systematic fine mapping of the complete Lith6 region is required to identify the causative genetic variants for gallstone in mice and humans[ 42 ]. From quantitative trait locus mapping in inbred mice, Kovacs P jeperawatan al[ 43 ] identified the Nr1h4 gene encoding the nuclear bile salt colelithiasis FXR farnesoid X receptor as a candidate gene for the cholesterol gallstone susceptibility locus Lith7. Genome wide scans of inbred strains of mice have linked the azuhan encoding the hepatocanalicular cholesterol transporter.
Supersaturation of bile with cholesterol is a primary step in the formation of cholesterol gallstones. The function of this transporter and the results of the genetic study taken together indicate that in gallstone-susceptible carriers of the ABCG8 19H allele, cholesterol cholelithiasis is secondary to increased hepatobiliary cholesterol secretion[ 44 ].
The formation of GS, supersaturated with cholesterol in bile, is determined by genetic and environmental factors. The genes associated with the development of GD are assumed to be located mainly on chromosomes 3, 4, 9 and 11[ 47 ]. The increased expression keperawatsn 3-hydroxymethylglutaryl-coenzyme-A-reductase, the enzyme that regulates the synthesis of cholesterol in the body, has been earlier suggested to play the most major role[ 48 ].
Gene variants in the lipid metabolism aeuhan contribute to the risk of biliary tract stones and cancers, particularly of the bile duct[ 49 ]. With certain gene polymorphisms, there is an increased risk for systemic metabolic disturbances, leading to the higher secretion of cholesterol into the bile kepsrawatan to gallbladder dysfunction[ 174446 ].
Genetic polymorphisms in apolipoprotein genes may be associated with alteration in lipid profile and susceptibility to GD[ 550 ].
Haplotype analysis is a better predictor of risk for GD[ 51 ]. It was asuhann presented that a common polymorphism in the cholelighiasis lipoprotein receptor-related protein-associated protein LRPAP1 gene might be associated with GD[ 52 ]. Mutations of the gene encoding the hepatocanalicular phosphatidylcholine transporters may lead to reduced lecithin secretion into the bile and its increased lithogenicity[ 5354 ].
Cholesterol 7alpha-hydrolase CYP7A1 is an enzyme that catalyzes the first, rate-limiting reaction of a cholesterol catabolic pathway. Recently, a common c. Mucin, a major component of mucus, plays an important role in GS formation. The molecular mechanisms of mucin overproduction, however, still remain unknown.
MUC5AC may be related to mucus hypersecretion[ 55 ]. These genes can work jointly to further increase susceptibility to GS in a Chinese population[ 56 ]. Being overweight and obesity: Being overweight and obesity are important risk factors of cholelithiasis[ 24313357 ]. Obesity is accompanied by increased synthesis and excretion of cholesterol into bile. At the same time, the amount of produced cholesterol is directly proportional to being overweight[ 8 ].
Larger weight fluctuation and more weight cycles are associated with greater risk[ 58 ]. The beta3-adrenergic receptor ADRB3 is a transmembrane receptor highly expressed in adipose tissue and thought to be involved in the regulation of lipolysis.
ADRB3 is also highly expressed in gallbladder tissue where it may be involved in gallbladder contraction. Klass et al[ 59 ] indicate that the ADRB3 Trp64Arg polymorphism is associated with gallstone disease, thereby representing a genetic marker that identifies subjects cholelithaisis higher risk for gallstone formation.
In the case of bypass surgery for obesity, the likelihood of cholelithiasis is even higher: Weight loss is accompanied by the elevated levels of mucin and calcium in the cystic bile, thereby giving rise to biliary sludge and stones in the gallbladder. A high intake of cholesterol increases its bile level[ 31 ]. A low-fiber diet slows wsuhan of the intestinal contents, which promotes the increased formation and absorption cholelithiassi secondary bile acids and the enhanced lithogenic properties of bile[ 22 ].
Refined carbohydrates increase cholesterol saturation of bile while small doses of alcohol have the opposite effect.