Podcast
Questions and Answers
What is the primary trigger for celiac disease (CD) in genetically predisposed individuals?
What is the primary trigger for celiac disease (CD) in genetically predisposed individuals?
- Inflammation of the gallbladder
- Autoimmune response to gut bacteria
- Viral infections affecting the small intestine
- Intake of gluten (correct)
Which genetic factors are most relevant in predisposing individuals to celiac disease?
Which genetic factors are most relevant in predisposing individuals to celiac disease?
- Mutations affecting intestinal permeability
- Polymorphisms in genes regulating bile acid synthesis
- Variations in the MHC-DR4 heterodimers
- Allelic variants related to MHC-DQ2 and/or MHC-DQ8 heterodimers (correct)
Which of the following HLA-DQB1 alleles is most strongly associated with celiac disease predisposition?
Which of the following HLA-DQB1 alleles is most strongly associated with celiac disease predisposition?
- HLA-DQB1*0301
- HLA-DQB1*0101
- HLA-DQB1*0402
- HLA-DQB1*02 (correct)
What is the typical outcome of gallbladder impairment in CD patients who adhere to a gluten-free diet?
What is the typical outcome of gallbladder impairment in CD patients who adhere to a gluten-free diet?
Why might the correlation between celiac disease and gallbladder complications be underestimated in current clinical understanding?
Why might the correlation between celiac disease and gallbladder complications be underestimated in current clinical understanding?
What type of study is needed to better understand the clinical implications of gallbladder alterations in CD patients?
What type of study is needed to better understand the clinical implications of gallbladder alterations in CD patients?
What does the statement 'this genetic background is necessary, but not sufficient, to develop CD upon gluten dietary exposure' imply?
What does the statement 'this genetic background is necessary, but not sufficient, to develop CD upon gluten dietary exposure' imply?
In the context of the article, what is the significance of MDPI staying neutral with regard to jurisdictional claims?
In the context of the article, what is the significance of MDPI staying neutral with regard to jurisdictional claims?
What did Low-Beer et al. initially observe in CD patients regarding gallbladder function?
What did Low-Beer et al. initially observe in CD patients regarding gallbladder function?
The study of bile salt turn-over in CD patients by Low-Beer et al. revealed what phenomenon?
The study of bile salt turn-over in CD patients by Low-Beer et al. revealed what phenomenon?
What did Di Magno et al. indirectly suggest was impaired in CD patients after a meal?
What did Di Magno et al. indirectly suggest was impaired in CD patients after a meal?
What key observation did Low-Beer et al. make regarding CCK levels in CD patients compared to controls?
What key observation did Low-Beer et al. make regarding CCK levels in CD patients compared to controls?
What method did Low-Beer et al. use to assess gallbladder response in conjunction with measuring plasma CCK kinetics?
What method did Low-Beer et al. use to assess gallbladder response in conjunction with measuring plasma CCK kinetics?
How did gallbladder emptying differ in CD patients compared to controls in the study by Low-Beer et al.?
How did gallbladder emptying differ in CD patients compared to controls in the study by Low-Beer et al.?
What is the significance of Low-Beer et al.'s work in understanding gallbladder dysfunction in CD patients?
What is the significance of Low-Beer et al.'s work in understanding gallbladder dysfunction in CD patients?
Based on the experimental study by Di Magno et al. and the work of Low-Beer et al., what is the proposed sequence of events leading to gallbladder dysfunction in CD patients?
Based on the experimental study by Di Magno et al. and the work of Low-Beer et al., what is the proposed sequence of events leading to gallbladder dysfunction in CD patients?
What does the analysis of available studies primarily suggest about the relationship between celiac disease (CD) and gallbladder function?
What does the analysis of available studies primarily suggest about the relationship between celiac disease (CD) and gallbladder function?
What is the potential long-term consequence of untreated celiac disease (CD) with regards to gallbladder function?
What is the potential long-term consequence of untreated celiac disease (CD) with regards to gallbladder function?
A study analyzes duodenal biopsies from patients with celiac disease (CD) and healthy controls. What is the primary conclusion regarding CCK-producing cells, based on immuno-staining and mRNA expression analysis?
A study analyzes duodenal biopsies from patients with celiac disease (CD) and healthy controls. What is the primary conclusion regarding CCK-producing cells, based on immuno-staining and mRNA expression analysis?
What correlation was observed between delayed celiac disease (CD) diagnosis and gallbladder ejection fraction (GBEF)?
What correlation was observed between delayed celiac disease (CD) diagnosis and gallbladder ejection fraction (GBEF)?
A researcher is investigating serum CCK8 concentrations in children with untreated celiac disease (uCD) after a fatty meal, using radioimmunoassay. How would one describe the expected CCK response in these patients compared to healthy controls?
A researcher is investigating serum CCK8 concentrations in children with untreated celiac disease (uCD) after a fatty meal, using radioimmunoassay. How would one describe the expected CCK response in these patients compared to healthy controls?
In the context of celiac disease (CD) and gallbladder function, what is the effect of adherence to a gluten-free diet (GFD)?
In the context of celiac disease (CD) and gallbladder function, what is the effect of adherence to a gluten-free diet (GFD)?
Two studies investigate CCK release in Celiac Disease (CD) patients. One analyzes duodenal biopsies via immunostaining and mRNA expression, while the other measures serum CCK8 concentration after a fatty meal. What is a key difference in methodology between these studies?
Two studies investigate CCK release in Celiac Disease (CD) patients. One analyzes duodenal biopsies via immunostaining and mRNA expression, while the other measures serum CCK8 concentration after a fatty meal. What is a key difference in methodology between these studies?
In studies assessing enteroendocrine cells, what inconsistent findings have been reported regarding CCK-positive cells in untreated celiac disease (CD) patients?
In studies assessing enteroendocrine cells, what inconsistent findings have been reported regarding CCK-positive cells in untreated celiac disease (CD) patients?
Based on the presented information, what conclusion can be drawn about the cause of defective CCK release in Celiac Disease (CD) patients?
Based on the presented information, what conclusion can be drawn about the cause of defective CCK release in Celiac Disease (CD) patients?
A researcher aims to replicate the findings of Deprez et al. (2002b) regarding CCK in celiac disease. Which methodologies would be most appropriate?
A researcher aims to replicate the findings of Deprez et al. (2002b) regarding CCK in celiac disease. Which methodologies would be most appropriate?
What was the main finding when comparing children with normal gallbladder ejection fraction (GBEF) to those with reduced GBEF in the subgroup analysis?
What was the main finding when comparing children with normal gallbladder ejection fraction (GBEF) to those with reduced GBEF in the subgroup analysis?
Consider two studies: Study A examines duodenal biopsies and Study B measures serum CCK after a fatty meal. If both studies involve children with untreated celiac disease (uCD), what confounding factor might disproportionately affect the results of Study B compared to Study A?
Consider two studies: Study A examines duodenal biopsies and Study B measures serum CCK after a fatty meal. If both studies involve children with untreated celiac disease (uCD), what confounding factor might disproportionately affect the results of Study B compared to Study A?
Based on the information, what parameters are indicative of gallbladder dysmotility in children with celiac disease?
Based on the information, what parameters are indicative of gallbladder dysmotility in children with celiac disease?
What statistical findings are reported concerning the delay in diagnosis and its impact on gallbladder function?
What statistical findings are reported concerning the delay in diagnosis and its impact on gallbladder function?
A new study aims to determine if a specific dietary intervention can improve CCK release in children with celiac disease. Based on the information provided in the text, which outcome would provide the STRONGEST evidence that the dietary intervention is effective?
A new study aims to determine if a specific dietary intervention can improve CCK release in children with celiac disease. Based on the information provided in the text, which outcome would provide the STRONGEST evidence that the dietary intervention is effective?
A researcher hypothesizes that the "flat intestinal mucosa" observed in some celiac disease patients directly impairs CCK release. Which of the following experimental approaches would be the MOST appropriate for testing this hypothesis in vitro?
A researcher hypothesizes that the "flat intestinal mucosa" observed in some celiac disease patients directly impairs CCK release. Which of the following experimental approaches would be the MOST appropriate for testing this hypothesis in vitro?
Which diagnostic finding is MOST indicative of chronic cholecystitis when using gallbladder scintigraphy?
Which diagnostic finding is MOST indicative of chronic cholecystitis when using gallbladder scintigraphy?
A patient presents with recurrent biliary pain, nausea, and bloating. Ultrasonography reveals gallbladder wall thickening. Which condition should be considered in the differential diagnosis, especially if the patient also has celiac disease (CD)?
A patient presents with recurrent biliary pain, nausea, and bloating. Ultrasonography reveals gallbladder wall thickening. Which condition should be considered in the differential diagnosis, especially if the patient also has celiac disease (CD)?
What is a key limitation in understanding the relationship between dyspeptic symptoms, right upper abdominal pain, and gallbladder contractility in celiac disease (CD) patients?
What is a key limitation in understanding the relationship between dyspeptic symptoms, right upper abdominal pain, and gallbladder contractility in celiac disease (CD) patients?
According to the 'UK biobank' study, what percentage of individuals with celiac disease (CD) were diagnosed with cholelithiasis?
According to the 'UK biobank' study, what percentage of individuals with celiac disease (CD) were diagnosed with cholelithiasis?
In the 'UK biobank' study, how did the rate of cholelithiasis in individuals with celiac disease (CD) compare to the control group?
In the 'UK biobank' study, how did the rate of cholelithiasis in individuals with celiac disease (CD) compare to the control group?
What is a primary challenge in diagnosing chronic cholecystitis?
What is a primary challenge in diagnosing chronic cholecystitis?
How might coeliac disease contribute to the development of cholesterol gallstone disease?
How might coeliac disease contribute to the development of cholesterol gallstone disease?
Why might gallbladder dysfunction contribute to abdominal symptoms in patients with celiac disease (CD)?
Why might gallbladder dysfunction contribute to abdominal symptoms in patients with celiac disease (CD)?
What percentage of individuals with celiac disease (CD) were diagnosed with unspecified cholecystitis in the 'UK biobank' study?
What percentage of individuals with celiac disease (CD) were diagnosed with unspecified cholecystitis in the 'UK biobank' study?
Which of the following is a potential complication of impaired gallbladder emptying?
Which of the following is a potential complication of impaired gallbladder emptying?
What could be a possible cause of acute acalculous cholecystitis in children, according to the text?
What could be a possible cause of acute acalculous cholecystitis in children, according to the text?
In critically ill patients, impaired gallbladder emptying is assessed using which diagnostic method?
In critically ill patients, impaired gallbladder emptying is assessed using which diagnostic method?
How does Peptide YY (PYY) affect gallbladder emptying in humans?
How does Peptide YY (PYY) affect gallbladder emptying in humans?
Why might elderly patients with biopsy-defined coeliac disease present a diagnostic challenge?
Why might elderly patients with biopsy-defined coeliac disease present a diagnostic challenge?
What is the significance of age at diagnosis in the nutritional course of coeliac disease?
What is the significance of age at diagnosis in the nutritional course of coeliac disease?
What is the likely connection between critical illness and impaired gallbladder emptying?
What is the likely connection between critical illness and impaired gallbladder emptying?
Flashcards
ref.
ref.
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n
n
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yrs.
yrs.
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Y
Y
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n/a
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Celiac Disease (CD)
Celiac Disease (CD)
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Genetic Predisposition in CD
Genetic Predisposition in CD
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Key HLA-DQB1 Alleles in CD
Key HLA-DQB1 Alleles in CD
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Gallbladder Impairment in CD
Gallbladder Impairment in CD
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Gallbladder Complications in CD
Gallbladder Complications in CD
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Need for Clinical Studies
Need for Clinical Studies
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Reversibility with Diet
Reversibility with Diet
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Improvements in CD Diagnosis
Improvements in CD Diagnosis
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What is CCK?
What is CCK?
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What is Immuno-staining?
What is Immuno-staining?
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What is uCD?
What is uCD?
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What is gfdCD?
What is gfdCD?
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What are IELs?
What are IELs?
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What is mRNA expression?
What is mRNA expression?
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What is Radioimmunoassay?
What is Radioimmunoassay?
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What is CMPE?
What is CMPE?
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Chronic Cholecystitis
Chronic Cholecystitis
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Symptoms of Chronic Cholecystitis
Symptoms of Chronic Cholecystitis
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Ultrasound Findings in Chronic Cholecystitis
Ultrasound Findings in Chronic Cholecystitis
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Gallbladder Scintigraphy in Chronic Cholecystitis
Gallbladder Scintigraphy in Chronic Cholecystitis
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Gallbladder Ejection Fraction Impact
Gallbladder Ejection Fraction Impact
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Overlap of Gallbladder Dysfunction
Overlap of Gallbladder Dysfunction
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Cholelithiasis Incidence in CD
Cholelithiasis Incidence in CD
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What is the 'UK biobank' (UKB)?
What is the 'UK biobank' (UKB)?
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GB dysmotility in CD
GB dysmotility in CD
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Reversing GB dysmotility
Reversing GB dysmotility
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Untreated CD & Gallstones
Untreated CD & Gallstones
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Delayed CD Diagnosis & GBEF
Delayed CD Diagnosis & GBEF
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CCK Release in CD
CCK Release in CD
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CCK-Positive Cells & CD
CCK-Positive Cells & CD
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Normal CCK cells in CD.
Normal CCK cells in CD.
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GFD and gall bladder motility
GFD and gall bladder motility
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Peptide YY & Gallbladder
Peptide YY & Gallbladder
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CCK Secretion in CD
CCK Secretion in CD
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CD Epidemiology
CD Epidemiology
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CD Diagnosis Age
CD Diagnosis Age
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CD in Asia
CD in Asia
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CD and Cholecystitis
CD and Cholecystitis
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Gallstones in CD Children
Gallstones in CD Children
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Gallbladder Emptying in Critical Illness
Gallbladder Emptying in Critical Illness
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Study Notes
- Celiac Disease (CD) is an immune-mediated disorder primarily affecting the small intestine, with potential impact on extra-intestinal organs, including liver and biliary tract.
Gallbladder Dysfunction in CD
- This review analyzes the pathophysiology and clinical evidence of gallbladder dysfunction in CD, focusing on potential complications and research gaps.
- CD patients may experience perturbations in bile composition and gallbladder dysmotility, mainly impaired emptying during digestion.
- A key factor is a perturbation of cholecystokinin secretion by duodenal enteroendocrine cells due to nutrient stimulation.
- Gluten-free diets appear to reverse this situation in most cases.
- CD patients don't show an increased predisposition to gallbladder complications like calculous and acalculous cholecystitis.
- Limited clinical studies have focused on these aspects, with recent improvements in CD diagnosis and treatment potentially reducing the impact of gallbladder dysfunction.
- There is a need for focused clinical studies for a comprehensive understanding of gallbladder alterations in CD.
Introduction to CD
- CD is triggered by gluten intake in genetically predisposed individuals with specific HLA-DQ variants, mainly MHC-DQ2 and/or MHC-DQ8 heterodimers.
- HLA-DQB1 alleles, particularly HLA-DQB102 and HLA-DQB10302, are most relevant for CD predisposition, though genetic background alone is insufficient.
- Additional factors like epigenetics and environment, greatly contribute to CD etiopathogenesis.
- The hallmark of CD is gluten-sensitive enteropathy, characterized by intraepithelial lymphocyte infiltration and villous atrophy in the small intestine.
- Liver is one of the most frequently affected extra-intestinal targets in CD, and unexplained hypertransaminasemia with non-specific histologic hepatic changes is the most common hepatic presentation of CD.
- Besides the liver, the biliary tract can also be affected in CD patients, causing changes in gallbladder function.
Gallbladder Anatomy and Function
- The gallbladder concentrates bile, adjusting its composition by absorbing water, sodium, cholesterol, phospholipids, and hydrophilic proteins and secreting mucins, hydrogen/chloride ions, immunoglobulins, and calcium.
- Bile acids in the gallbladder bile have a greater concentration than in hepatic bile.
- Synthesized from cholesterol in the liver, bile acids are conjugated to taurine or glycine for increased solubility, then concentrated and stored in the gallbladder.
- The gallbladder consists of the fundus, corpus, and infundibulum, ending in the cystic duct that joins the common bile duct without a sphincter.
- The common bile duct merges with the pancreatic duct, forming the ampulla of Vater which opens into the duodenal lumen with the sphincter of Oddi.
- Innervated by vagal and splanchnic nerves, the gallbladder is functionally integrated with the digestive tract through neuro-hormonal mechanisms.
- Bile flows through passive and active means during fasting, with adrenergic and non-adrenergic fibers facilitating relaxation for bile reception.
- Contractions during the cephalic, antral, and intestinal phases are due to the nerves and gut hormone cholecystokinin (CCK), while the Sphincter of Oddi relaxes.
- Cephalic and antral gallbladder emptying is nervouse mediated, while intestinal phase relies on CCK action.
CCK Production and Function
- CCK hormone is produced by I-cells of the intestinal mucosa, which have a close proximity to the intestinal lumen, enabling for efficient sensing.
- Luminal content, especially food rich in protein and fat, highly effects and stimulates CCK release .
- CCK secretory granules in the basal cell region contain a mixture of molecular forms; CCK-33 is predominant in the human intestine and circulation.
- By interacting with receptors, CCK peptides stimulate the target cells.
- CCK1 receptors mediate gallbladder contraction and relaxation of the sphincter of Oddi, along with hepatic bile, pancreatic enzyme secretion, growth, and inhibition of gastric acid secretion and emptying.
- CCK2 receptors are mainly in the brain.
Gallbladder Functioning and Regulation in CD
- CD's hallmark is the damage and flattening of the jejunal/ileal mucosa, potentially impairing endocrine cells.
- Intestinal injury from CD can impair digestion and absorption, directly by enterocyte damage and villous architecture disruption, and indirectly, by disrupting the production and secretion of gut hormones and peptides that regulate gut motility and organs involved in digestion like the exocrine pancreas and gallbladder.
- Increased bile flow rate and biliary secretion of components like cholesterol, phospholipids, and bile acids reported in active CD, return to normal under GFD.
- Cholesterol secretion into bile is linked to a decrease in serum cholesterol in CD, observed in both children and adults.
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