Hepatobilliary Flashcards
Alcohol liver disease
Description, types, manifestations
Liver damage caused by excessive consumption of alcohol
* Alcohol is metabolised to acetylaldehyde, toxic to hepatocytes
Types: Fatty liver (asymptomatic & reversible), alcoholic hepatitis (inflammation and onset of fibrosis), cirrhosis (irreversible fibrosis and necrosis)
Manifestations: fatigue, weightloss, adominal pain, ascites, GI haemorrhage, portal hypertension, hepatic encephalopathy, oesophageal varices
Hepatitis (Description, PP)
Inflammation of the liver most commonly caused by various strains of the hepatitis virus A, B, C
PP: hepatic cell necrosis, Kupffer cell hyperplasia, infiltration of liver tissue by mononuclear phagocytes which obstructs bile flow and impairs hepatocyte function, jaundice
Increases risk of metastatic invasion of the liver
Manifestations of hepatitis
Stage 1 (pre-icteric): fever, malaise, anorexia, liver enlargement and tenderness
Stage 2 (icteric phase): jaundice, hyperbilirubinaemia, dark urine
Stage 3 (recovery): resolving symptoms, resolution of jaundice but liver still tender
Chronic hepatitis
Liver inflammation lasting >6 months
Complication of hepatitis virus B or C causing widespread necrosis and fatality
Portal hypertension
Description, causes, manifestations
Elevated portal venous blood pressure caused by increased resistance to venous flow in the portal vein from the intestines
Caused by liver disease or obstruction
Manifestations: ascites (abdominal swelling & distension), hepatic encephalopathy, bleeding varices
Hepatic encephalopathy
Causes, manifestations
Impaired cerebral function caused by blood-borne toxins (e.g. ammonia) not being properly metabolised in the liver (diseased metabolites), or by bypassing the liver due to portal hypertension
Manifestations: confusion, memory loss, asterixis (flapping hand tremor), LOC, coma, death
Jaundice/Icterus
Types
Yellow/green pigmentation of the skin or sclera of the eyes caused by increased plasma bilirubin (hyperbilirubinaemia)
**Obstructive: **obstruction of bile canal (intrahepatic) or extraheptic causing proximal accumulation, enter into bloodstream and deposited in skin
Prehepatic: RBC destruction rate > bilirubin metabolism (monitor in newborns as persistance causes brain damage)
Neonatal: transient in the first few weeks due to normal Hb breakdown
Liver functions
- Metabolism of carbs, proteins and lipids
- Storage of glucose, lipids, minerals, vitamins, /hb
- Produce bile, clotting factorsm hormone precursors
- Detoxification, pathogen removal
Bile
Description, pathway and secretion
- Produced by hepatocytes that carries waste and breaksdown fats
- Contains bile salts, bile pigments (bilirubin), cholesterol, electrolytes, water
- Intrahepatic collecting system - L/R hepatic duct, common hepatic duct - cystic duct - gallbladder
- Eating stimulates hormone cholecystokinin, that contracts the bile duct, sending bile through cystic, into common, into duodenum
Cholelithiasis/gallstones
Description, PP, risk/aetiology, types
Calculi in the gallbladder due to bile aggregation of cholesterol crystals or precipitates of unconjugated bilirubin, that fill the gallbladder, or obstruct cystic or common bile duct
Manifestations: abdominal pain, jaundice
Risks: female, prenancy, oral contraceptives, obesity, bile stasis, dehydration (GB absorbs water)
Cholesterol stones: most common, usually made water soluble by combining with bile salts, but supersaturation of cholesterol causes precipitation (due to excessive cholesterol secretion in metabolic disorders or decreased bile salt in CF)
Brown pigment: soft and greasy, when bilirubin joins with calcium during infection, inflammation, parasitic infection
Cholecystitis
Description, types
Inflammation of the gallbladder due to trapped bile
Calculous: most common, caused by lodges stone in the cystic duct, where gallbladder becomes distended, and pressure reduces blood flow causing ischaemia, necrosis and perforation
Acalculous:
* stagnant noxious concentrated bile, most likely due to fasting and a lack of CCK stimulus
* Critical illness, major surgery, sepsis, immunocompromised
Clinical manifestations of cholecystitis
Acute, chronic, total obstruction
Acute
* Symptoms usually occur a few hours after high fat meal or when lying down
* Pain: severe, referred to shoulder
* RUQ tenderness and rigidity, esp a few hours after eating (colic-like)
* Tachycardia, fever, N/V, jaundice
Chronic
* fat intolerance, dyspepsia, heartburn, flatulence
Total obstruction (common bile duct)
* jaundice, dark urine, clay stool (fat), bleeding,
Complications of cholecystitis
- gangrene
- Biliary cirrhosis
- Rupture & peritonitis
- Abscess
- Pancreatitis
- Cholangitis (inflammation of bile ducts)
- Fistulas (stone erode through into duodenum and impacts ileus or obstruct gastric outlet)
- Empyema (pus pockets) due to bacterial proliferation causing severe fever and leukocytosis*
Diagnosis of cholecystitis
- History, physical exam, imaging studies (US, CT)
- Cholecystogram (X-ray) detects blockage
- Hepatobiliary iminodiacetic scan detects abnormal ejection
- ERCP: endoscopy retrograde cholangiopancretography (flurescence/isotope functional imaging)
Lab tests looking for high:
* WBC, serum & urinary bilirubin, (LFT) liver enzymes and serum amylase
* Blood cultures if high temp
Pregnancy screening for possible cause
Non surgical treatment of cholecystitis
- Pain: NSAIDs, morphine, anticholinergics (atropine)
- AB therapy
- oral dissolution medication
- Extracorporeal shock-wave lithotripsy (disintegrate stones)
- Fat soluble vitamins prevent stones
