Alcohol and diet in gallstone disease Flashcards
Name some gallbladder diseases
Cholelithiasis (GS disease)
Cholecystitis (acute and chronic) - blocking duct
Choledo-cholithiasis - blocking bile duct
Gallbladder cancer
Gangrene of GB
Abcess of GB
Gallbladder polyps
Acalculous GB disease
Biliary dyskinesia
Sclerosing cholangitis (inflamm and scarring of bile ducts)
How do gallstones develop?
- Bile contains unusually high levels of cholesterol or bilirubin or low levels of bile salts
- Gallbladder is dysfunctional
- Release of bile impaired
What are the two different types of stones?
Pigment (bilirubin) stones - main type in chronic haemolytic disorders or cirrhosis
Cholesterol stones - influenced by effects on more than one aspect of metabolic syndrome (obesity, IR, HTN, dislipidemia)
Role of body weight on gallstones
Obesity - acts on most mechanisms of formation e.g. super saturation of bile with cholesterol
Rapid weight loss - cholecystectomy in a third of bariatric patients - risk minimised by ursodeocycholic acid
Role of physical activity
Regular PA protects against formation and limits symptomatic stones by 30%
Mechanisms include decreased insulin and insulin resistance, increased plasma HDL during PA suggesting increase in cholesterol transport back to liver, stimulating GB contraction
Role of diet in GS
Limit dietary fat but not very low fat diet, evidence mixed for veg diets/coffee/alcohol, regular eating patterns, fibre and calcium, PUFA/MUFA, fruits and veg, vit C
Liver disease - damage of cells leads to…
Hepatitis
Fibrosis
Cirrhosis
Hepatocellular carcinoma
What is NAFLD and what are risks?
Significant fat accumulation of hepatocytes in absence of alcohol intake or other causes of LD
RFs are obesity (driven bu IR mainly)
Lifestyle approach for NAFLD
calorie restriction, abstain from alcohol, physical activity, macronutrient composition (med diet helps, don’t offer omega 3), coffee consumption
Likely mechanisms of alcohol and cancer
Carcinogenic breakdown products e.g. acetylaldehyde
Oxidative stress - producing potentially genotoxic reactive oxygen species
Solvent - makes it easier for carcinogens to enter cells
Deficiencies in essential nutrients - makes tissue susceptible to carcinogenic effect
Explanations of alcohol and weight gain paradox
Differences in energy expenditure
Lots of confounders - gender, type of alcohol, physical activity level, sleeping habits, depression symps, psychosocial problems, chronic illness, meds
Tendency to binge
Inaccuracies in reporting
How can alcohol increase risk of malnutrition?
Replacing food intake
Digestion - dec secretion of pan enzymes and bile
Absorption - damage of cells lining SI and stomach
Metabolism - relies o micronutrients e.g. thiamine
Nutrient transport, storage and excretion - dec liver stores of vits (e.g vit A) and inc secretion (inc fat)
Secondary malnutrition - chronic pancreatitis and liver disease, infection and injury, ascites can dec appetite
Sarcopenia (muscle mass loss) in alcohol induced liver disease
Preferential use of lipids as a fuel (fat loss) and dec protein synthesis (muscle atrophy) in heavy drinkers
Susceptibility to infections, ascites
protein energy malnutrirtion common - screen all with cirrhosis e.g. MUST, adjusting for fluid retention
If emd or high risk detailed assessment by dietitian
Common deficiencies in ALD
Thiamine (B1)
Important in ATP production, normal nerve conduction, maintenance of neural membranes
Levels rapidly reduce in chronic alcohol use due to poor intake, dec conversion to coenzyme, dec storage in fatty liver, inhibited int absorption, inc metabolic demand - use of thiamine for ethanol metabolism
Clinical signs of deficiency
Nervous system - weakness, numbness, paralysis
CVS - ic HR, SOB, high output cardiac failure
wernicke-Korsakoff syndrome (spectrum) - Wernickes encephalopathy - reversible if identified early, Korsakoff - mostly irreversible
