Hepatic Disorders Flashcards
what is jaundice?
yellow discolouration of the skin and sclera d/t excess serum bilirubin (40umol/L, 3mg/dL)
not necessarily liver disease
what types of jaundice are there?
conjugated and unconjugated
obstructive and non-obstructive (clinical)
pre-hepatic, hepatic and post-hepatic
example of post hepatic jaundice
could be due to tumors or stones
what is pruritus caused by in jaundice?
cutaneous fat deposits d/t malabsorption
what class of meds is not admin in jaundice?
antihistamines bc you have a compromised liver
important teaching point with jaundice
keep skin clean and moisturized
obstructive jaundice
~biliary atresia; biliary disease or blockage d/t inflmtn
~gallstones - cholestatic meds can cause internal blockage of ducts
~bile can’t flow into intestines and backs up in liver and blood, staining skin, sclera, and urine bright orange and frothy
~stool is clay-coloured and skin is itchy
~intolerance of fatty foods; you will have fatty stools
~AST, ALT and GGT levels rise moderately, but alkaline phosphatase and bilirubin levels are elevated
~post hepatic (stones, tumors) - urine is high coloured
hepatocellular jaundice
- viral, alcohol, toxins, drugs
- liver damage is unconjugated
- swelling, canicular obstruction is conjugated
- liver unable to clear bilirubin d/t damage
- can be d/t: infection, toxins, meds, alcohol, obesity
- AST and ALT levels may be increased (indicates cell necrosis)
- may be reversible unless cirrhosis develops
- serum bilirubin and urobilinogen levels may be elevated
if cause of hepatocellular jaundice is infectious, what manifestations will occur in the pt?
headache, chills, fever
hemolytic jaundice
- result of inc destruction of RBCs, effect of which is to flood plasma w/ bilirubin so rapidly that liver can’t excrete bilirubin as quickly as it is made
- in pts with hemolytic transfusion rxns and hemolytic disorders
- fecal and urine urobilinogen levels are inc, but urine is free of bilirubin
- predisposes to formation of pigment stones and extremely severe jaundice
- bilirubin levels >300-400umol/L causes brainstem damage
hereditary hyperbilirubinemia jaundice
- serum bilirubin increases but LFT and liver histology remains normal
- Gilbert’s syndrome : familial disorder characterized by increased level of unconjugated bilirubin
- affects 3-8% of population (mainly males)
portal HTN
- increased pressure throughout the portal venous system that results from obstruction of blood flow through the liver
- associated with hepatic cirrhosis
- changes in clotting increase risk of bleed
what is portal HTN caused by?
- portosystemic shunts
- ascites - d/t liver and kidney disease, CA, and heart failure
- varices - risk for GI bleed (upper, rectal)
- splenomegaly
portal HTN is a result from…
circulatory changes w/in diseased liver and produces severe GI hemorrhages and marked Na+/fluid retention
contributing factors of ascites
portal HTN and obstruction of venous blood flow to liver
patho of ascites
movement of fluid from vascular system into peritoneal space is d/t: Na+/H2O retention inc intravascular fluid vol inc lymphatic flow dec synthesis of albumin
why do you have sodium and water retention?
liver can’t metabolize aldosterone, so kidneys retain these things
how much fluid accumulates in ascites?
15L of albumin-rich fluid accumulates in peritoneal cavity and if you increase portal pressure, you will have movement of fluid into peritoneal cavity
treatment of ascites
- dietary modification (restrict Na and fluids)
- diuretics (spironolactone and lasix)
- bed rest (upright position to activate RAAS and SNS)
- paracentesis (admin of albumin to shift fluid from IS to vascular space)
- TIPS (Transjugular Intrahepatic Portosystemic Shunt)
things to remember about diuretics
- when used with other diuretics, helps prevent potassium loss
- long term use of oral diuretics can cause hyponatremia
- daily weight loss should not exceed 1-2kg in pts with ascites and peripheral edema or 0.5-0.75kg in pts without edema
- fluid restriction is not attempted unless serum sodium [ ] is very low
how would you go about making dietary modifications for someone with ascites and impaired renal fx?
avoid salt substitutes containing potassium
other methods of treating ascites?
insertion of peritoneovenous shunt to redirect ascitic fluid from peritoneal cavity into systemic circulation
pitting edema
hypoalbuminemia d/t dec hepatic production of albumin
nutritional deficiencies
inability of the damaged liver cells to metabolize certain vitamins leading to:
- Impaired fxing of the central and peripheral nervous system - Abnormal bleeding tendencies
Korsakoff syndrome
- chronic, memory disorder and is caused by lack of thiamine (vitamin B1), which affects the brain and nervous system
- most commonly caused by alcohol misuse, but certain other conditions can also cause it
what happens with people who drink lots of alcohol?
- people who drink excessive amounts of alcohol are often thiamine deficient - bc many heavy drinkers have poor eating habits and their diet does not contain essential vitamins
- alcohol can interfere with the conversion of thiamine into the active form of the vitamin
disadvantages of alcohol on the body
- can inflame the stomach lining and cause frequent vomiting and make it difficult for the body to absorb key vitamins it receives
- also makes it harder for the liver to store vitamins
decreased synthesis
Hepatic encephalopathy:
- d/t accumulation of ammonia in the serum d/t impaired protein metabolism
esophageal varices
- develop in majority of pts with cirrhosis
- tortuous veins in the submucosa of the lower esophagus but can be in the higher esophagus and extend into the stomach
cause of esophageal varices
- d/t portal HTN; variscosities that develop from increased pressure in veins that drain into portal system. increased obstruction of the portal vein causes venous blood to take alt route to the right atrium, inc pressure in vessels of submucosal layer
- vessels are not elastic = fragile and will bleed easily
