INP midterm - LIVER Flashcards
Flashcards for the first half of the INP course. This set will cover the LIVER
What are the primary functions of the liver?
1) Bile – secretion and excretion
2) Infection – globulins and complement (fights infections)
3) Oncotic Pressure - makes albumin and transferrin
4) Lipid Metabolism – digests and absorbs lipids
5) Glucose Homeostasis – through glycogenesis, glycogenolysis, and gluconeogenesis
6) Coagulation – makes fibrinogen, clotting factors, and vitamin K
7) Detoxification – conjugation, degradation, NH3 & urea
What are some of the reasons why a person with liver disease would be malnourished?
–> Decreased intake of nutrients
–> Early satiety
–> Increased losses of nutrients, minerals, vitamins
–> Malabsorption – fat, bile acid deficiency
–> Hypermetabolic state
What are the nutrition considerations for patients with acute liver injury?
–> Catabolism exceed anabolism
–> Carbohydrates become preferred source of energy
–> Need adequate protein delivery to avoid muscle breakdown and as a substrate for gluconeogenesis
–> Favorable nitrogen balance
–> Early enteral nutrition reduced infectious complications
–> Meet full calorie need by no more than a week
What are the nutrition considerations for patients with chronic liver disease?
–> Early parenteral nutrition may increase infection
–> Obese patient may trend towards lower calories and increased protein
–> Delayed clearance of NH3 from protein metabolism can exacerbate hepatic encephalopathy
–> Excessive fluids (liver senses low fluid and retains more solvent) – herniation
–> Parenteral nutrition additive toxicity to live
–> Protein needs 25-50% higher than baseline (bad – low branch chain to aromatic amino acid ratio)
What are the nutritional recommendations given to patients with chronic liver disease?
–> Eat small and frequent meals to avoid fasting
–> Consume high complex carbs - 35-40 kcal/body kg/day
–> Consume BCAA enriched formulas
What is nonalcoholic fatty liver disease (NAFLD)?
Macrovesicular fat in >5% of hepatocytes in the absence of: significant alcohol, drugs, toxins, viral hepatitis, TPN, metabolic errors, cystic fibrosis, Wilson’s Disease
What is the clinical presentation of NAFLD?
–> MOST are asymptomatic
–> Insulin resistance (pre-diabetes)
–> Obesity
–> Hypertension
–> Dyslipidemia
–> accelerated atherosclerotic heart disease
Describe the pathogenesis of NAFLD.
1) TG accumulation - excessive import of free FA but decreased hepatic export, and impaired B-oxidation
2) Insulin resistance - genetic basis unclear; potential polymorphisms in apoprotein C3, IL-6, adipose tissue, or alteration in peroxisome promoter
3) hepatocellular injury - ROS, defects in mito oxidative phosphorylation, activation of proinflammatory cytokines/mediators
4) Antioxidant depletion – impaired T reg function (glutathione, Vit E, b-carotene, Vit C)
5) Iron – insulin resistance and increased hepatic iron, HFE gene more prevalent, iron stores correlate with fibrosis severity, may generate ROS in iron reduction process
6) Leptin – decreased leptin production from adipose leads to obesity, may contribute to fibrosis, CNS effects
7) Adiponectin – beneficial adipose hormone
enhances plasma lipid clearance, FFA metabolism in muscle
suppresses TNF-alpha (anti-inflammatory effect)
8) Resistin – adipose-derived protein that leads to insulin resistance
9) Intestinal microbes – altered intestinal permeability, endogenous alcohol and acetaldehyde production, endotoxin production, deconjugation of bile salts
How is NAFL(Non-alcoholic Fatty Liver)/NASH diagnosed?
–> Imaging (enlarged liver), labs (AST and ALT NASH has higher ALT, elevated ferritin, auto-immune markers)
–> Liver biopsy
How is the severity of NAFL/NASH measured?
- -> Radiographic findings:
* Sonogram – increased brightness
* CT scan – decreased hepatic attenuation
* MRI – increased fat signal
* MR spectroscopy
Summarize the treatment options for NAFLD. In particular, what dietary interventions have been shown to be beneficial?
- -> Lifestyle modification
- -> Drugs:
* Vitamin E– decreases oxidative stress
* Insulin sensitizing agents (thiazoldinediones, metformin)
* Omega-3 fatty acids
Vitamin E has been found to be the most beneficial
Who needs a liver transplant?
–> people with liver failure (loss of function)- coagulopathy, encephalopathy, cholestasis
–> cancer patients
- -> people with structural-related complications such as:
* Ascites (excess free fluid)
* Portal hypertensive bleeding
* Hepatorenal syndrome
* Hepatopulmonary syndrome
What are the benefits of a living donor liver transplant?
–> Timing of procedure
–> No graft ischemia
–> Potential long term immunological advantages
–> Bonding experience
What are some of the problems with a living donor liver transplant?
–> Small risk to donor
–> Reduced size graft
What are the common complications affecting people with liver transplants?
–> Obesity (major one)
–> Hyperglycemia
–> Bone disease
–> Growth failure
–> Hyperlipidemia
–> Minimizing/eliminating steroids
–> Drinking