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Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
Dr Devendra Sancheti gallstone disease
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Dr Devendra Sancheti gallstone disease

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powerpoint presentation of gall bladder disease

powerpoint presentation of gall bladder disease

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  • 1. Presented by Vd. Devendra Sancheti Guide Dr.R.R.Patil HOD ROGNIDAN DEPARTMENT
  • 2.  Types of gallstone  Cholesterol stones (20%)  Pigment stones (5%)  Mixed (75%)  Epidemiology  Fat, Fair, Female, Fertile, Fourty inaccurate, but reminder of the typical patient  F:M = 2:1  10% of Indian women in their 40s have gallstones
  • 3.  Composition of bile:  Bilirubin (by-product of haem degradation)  Cholesterol (kept soluble by bile salts and lecithin)  Bile salts/acids (cholic acid/chenodeoxycholic acid): mostly reabsorbed in terminal ileum(entero-hepatic circulation).  Lecithin (increases solubility of cholesterol)  Inorganic salts (sodium bicarbonate to keep bile alkaline to neutralise gastric acid in duodenum)  Water (makes up 97% of bile)
  • 4.  Cholesterol  Imbalance between bile salts/lecithin and cholesterol allows cholesterol to precipitate out of solution and form stones  Pigment  Occur due to excess of circulating bile pigment (e.g. Heamolytic anaemia)  Mixed  Same pathophysiology as cholesterol stones  Other Factors  Stasis (e.g. Pregnancy)  Ileal dysfunction (prevents re-absorption of bile salts)  Obesity and hypercholesterolaemia
  • 5. 80% Asymptomatic  20% develop complications and do so on recurrent basis 
  • 6.  Gallstone disease (and its related complications) Gastritis/duodenitis Peptic ulcer disease/perforated peptic ulcer Acute pancreatitis Right lower lobe pneumonia Miyocardial Infarction  If presenting with RUQ pain all patients should get       Blood tests  Abdominal xray / CXR (to exclude perforation/pneumonia)  ECG
  • 7.  Can differentiate between gallstone complications based on:  History  Examination  Blood tests  CBC  LFT  CRP  Clotting  Amylase
  • 8. Complication History Examination Blood tests Biliary Colic - Intermittent RUQ/epigastric pain (minutes/hours) into back or right shoulder -Tender RUQ -Murphy’s – -HR and BP (N) -Wbc (N) CRP (N) - LFT (N) Acute Cholecystitis -Constant RUQ pain into back or right shoulder -Feverish -Tender RUQ -Murphy’s + -Pyrexia, HR (↑) -Wbc and CRP (↑) -LFT (N or mildly (↑) Empyema -Constant RUQ pain into back or right shoulder -Feverish -Tender RUQ -Murphy’s + -Pyrexia, HR (↑), BP (↔ or ↓) -More septic than acute cholecystitis -Wbc and CRP (↑) -LFT (N or mildly (↑) Obstructive Jaundice -Yellow discolouration -Pale stool, dark urine -painless or associated with mild RUQ pain -Wbc and CRP (N) -LFT: obstructive pattern bili (↑), ALP (↑), GGT (↑), ALT/AST (↔) -INR (↔ or ↑) Ascending Cholangitis Becks triad -RUQ pain (constant) -Jaundice -Rigors Gallstone Ileus - 4 cardinal features of Small Bowel Obstruction -Jaundiced -Non-tender or minimally tender RUQ -No peritonism -Murphy’s – -Apyrexial, HR and BP (N) -Jaundiced -Tender RUQ -Peritonism RUQ -high pyrexia (38-39) -HR (↑), BP (↔ or ↓) -Can develop septic shock -distended tympanic abdomen -hyperactive/tinkling bowel sounds -Wbc and CRP (↑) -LFT : obstructive pattern bili (↑), ALP (↑), GGT (↑), ALT/AST (↔) -INR (↔ or ↑)
  • 9.         Blood Tests Abdominal Xray (10% gallstones are radio-opaque) Chest Xray (to exclude perforation – MUST!) ECG (to exclude MI) Ultrasound Sonography: first line investigation in gallstone disease  Confirms presence of gallstones  Gall bladder wall thickness (if thickened suggests cholecystitis)  Biliary tree calibre (CBD/extrahepatic/intrahepatic) – if dilated suggests stone in CBD (normal CBD <8mm).  Sometimes CBD stone can be seen. MRCP: To visualise biliary tree accurately (much more accurate than ultrasound)  Diagnostic only but non-invasive  Look for biliary dilatation and any stones in biliary tree ERCP: Diagnostic and therapeutic in biliary obstruction  Diagnostic and therapeutic but invasive  Look for biliary tree dilatation and stones in biliary tree  Stones can be extracted to unobstruct the biliary tree and perform sphincterotomy  Risk of pancreatitis, duodenal perforation CT Abdomen: Not first line investigation. Mainly used if suspicion of gallbladder empyema, gangrene, or perforation and in acute pancreatitis (ultrasound not good for looking at pancreas)
  • 10. Pathogenesis  Stone intermittently obstructing cystic duct (causing pain) and then dropping back into gallbladder (pain subsides) Ultrasound confirms presence of gallstones
  • 11. Pathogenesis:  Due to obstruction of cystic duct by gallstone:  Cystic duct blockage by gallstone  Obstruction to secretion of bile from gallbladder  Bile becomes concentrated  Chemical inflammation initially  Secondarily infected by organisms released by liver into bile stream Ultrasound confirms diagnosis (gallstones, thickened gallbladder wall, peri-cholecystic fluid) Complications of acute cholecystitis  Empyema of gallbaldder  Gangrene of gallbladder (rare)  Perforation of gallbaldder (rare)
  • 12. Pathogenesis:  Stone obstructing CBD with infection/pus proximal to the blockage
  • 13. Pathogenesis:  Gallstone causing small bowel obstruction (usually obstructs in terminal ileum)  Gallstone enters small bowel via cholecysto-duodenal fistula (not via CBD) Abdominal Xray – dilated small bowel loops  May see stone if radio-opaque Diagnosis of gallstone ileus usually made at the time of surgery.
  • 14. Questions?
  • 15. THANK YOU

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