Hepatic Impairment Flashcards
(19 cards)
describe the blood supply to the liver
receives 1.3L of blood per minute.
dual supply- 20% from hepatic artery (aorta) and 80% from hepatic portal vein (gut)
what are the functions of the liver?
Metabolises- carbs proteins fats, bilirubin, thyrxine, drugs
Makes- Albumin, bile, clotting factors, cholestrol
Stores- Fat soluble vitamins ADEK and glycogen
Regulates- Blood glucose
Immunity- contains macrophages
what is acute liver disease?
symtopms for less than 6 months
what is chronic liver disease?
symptoms for greater than 6 months
what is the usual timeline of liver disease?
hepatitis (liver inflammation) and steatosis (fatty liver) (steatohepatitis). Liver can fully recover at these stages
Progresses to fibrosis (scar tissue formation) and eventually cirrhosis (extensive scar tissue- reduces blood flow)
What causes liver disease?
Alcohol- 80% of drinkers get fatty liver. Max 14 units per week, spread over 3+ days with free days
Viral Infection- Hep ABCDE
Non-Alcoholic Fatty Liver disease- Triglycerides build up in hepatocytes.
Drug Induced- NSAIDs, amiodarone, codeine, carbimzole, azathioprine, nitrofurantoin
Genetic- hameachromatosis
Immunological- Lupus/RA
Malignancy- hepatocellular carcinoma
What are the risk factors for liver disease?
Woman
Older
Genetics
Increased alcohol intake
Mr drug formulation
Polypharmacy
What are idiosynchratic drug reactions?
Spontaneous, not reproducible, not dose dependent
Methotrexate
What are symptoms of Liver Disease?
Finger clubbing- poor blood circulation
Jaundice- build up of bilirubin because liver doesnt break down
Fatigue, loss of appetite, weight loss
Bruising and bleeding- lack of clotting factors
Portal HTN and Varices- Reduced flow increases blood pressure in liver so forms weak collateral veins (varices) to bypass which can bleed
Encephalopathy- ammonia build up crosses CNS causing confusion, delerium, modified behaviour
Pale/fatty stools and dark urine-
Ascites- build up of ascitic fluid between the peritoneum in abdoen due to decreased sodium excretion
Gynaecomastia
Pruritus- build up of bile salts beneath the skin
Palmer erythrma and spider neavi
How is Portal HTN/Varices prevented and treated?
Prophylactic low dose propranolol- decrease HR by 25%. Low dose becausse propanolol undergoes extensive FPM. Omeprazole
Treat (active bleed)- Octreotide IV
How is Encephaloptahy treated?
Lactulose- travels to liver chemically unchanged, decreases the colon pH which traps ammonia and prevents being absorbed again. Acidic environment inhibits ammonia producing bacteria to grow.
Rifaximin- reduces ammonia producing bacteria growing
How is ascites treated?
Restricted dalt diet
Spironalactone max 400mg daily
Peritoneocentesis- mechanical drainage
How is pruritis treated?
Cholestyramine- binds the bile salts (WATCH- INTERACTIONS- ALSO BINDS DRUGS)
Antihistamine- ceterizine 10mg daily
How is liver function assessed?
Monitor-
- Albumin- decreased because not being made by liver.
- Prothrombin- long clot time means decreased clotting factors because not made by liver
-ALT and AST- found in hepatocytes so when damaged, leak out (increased levels). ALT more liver specific. Increased in hepatitis
-ALP and GGT- found in bile ducts. Raised GGT indicates alcohol (can raise after night out). Increased in choleostasis
-Bilirubin- Liver breaks down. From RBC breakdown. Pigment in Bile. Raised in jaundice
-Liver Ultrasound
-Liver biopsy
What is Child-Pugh Classification?
Indicates severity of liver cirrohsis
C= worst (10-15)- avoid kaftrio if C
Used in SPC for Citalopram
Considers ascites, encephalopathy, albumin, bilirubin, INR (high INR means less clotting factors being produced)
What drugs/classes should be used with caution or avoided in liver disease?
Constipating- can worse enceph. due to increased nitrates
Diuretics
GI ulceration causing- NSAIDs, aspirin
Can cause bleeding- warfarin, DOACs
Nephrotoxic- NSAIDs, Aminoglyc
High sodium content- soluble tabs, antacids
GI drugs- PPIs and H2 receptor antagonists
What are the PK changes in liver disease?
Absorption- Lipid sol drugs need bile for breakdown. Decreased bile in cholestasis so decreased fat absorption
Distribution- Decreased albumin made, so decreased binding and increased toxicity. Water sol drugs can go to ascitic fluid so need larger LOADING DOSE
Metabolism- decreased fpm so high oral bioavail= increased side effects or toxicity- AVOID HIGH FPM DRUGS AND PRO-DRUGS
Excretion- if biliary secreted, this is reduced in choleostasis so can lead to accumulation. If renally excreted, decrease dose.
USE SHORTER HALF LIFE DRUGS/NO MR MEDS
What is Cholestasis?
Blockage of bile flow. Bile needed to break down and absorb fats.
What are the PD changes in liver disease?
Patients more sensitive to renal SE’s of NSAIDs
Patients may have reduced response from some drugs due to poor metabolism of them
