2001 study

• Functions of the liver

  • Clearance (aldosterone, drugs)
  • Storage (vitamins, glycogen)
  • Homeostasis (glucose levels regulation)
  • Synthesis (albumin, clotting factors)
  • Metabolism (vitamin D)
  • Secretion (bile salts)
  • Excretion (cholesterol)
• Cirrhosis


  Chronic liver damage from a variety of causes leading to scarring and liver failure
• Portal hypertension


  • Increase pressure within the portal venous system. Cirrhosis slows down the blood flow and puts stress on the portal vein leading to heightened pressure
  • Beta blockers are first line of medication (reduce cardiac output) e.g. Propranolol
• Encephalopathy


  • CNS disturbance associated with hepatic insufficiency and liver failure
  • Drug therapy to reduce blood ammonia concentration, inhibition of GABA receptors e.g. Lactulose
• Ascites


  • The accumulation of lymph fluid in the peritoneal cavity. Less blood flow to the liver leads to albumin fluid leaking through capillaries
  • Reduce sodium and fluids, avoid NSAIDs e.g. Frusemide (loop diuretic)
• Hepatorenal syndrome


  • Progressive renal failure associated with cirrhosis. It is the gradual rise of creatine while urine output falls
  • Stop diuretics and NSAIDs, antibiotics, norfloxacin (vasopressin analogue)
• Functions of the kidneys

  • Remove waste products from the blood and produce urine
  • Water balance
  • Electrolyte balance
  • Acid base
  • Activation of vitamin B
• Steps in urine formation

  • Filtration
  • Reabsorption
  • Secretion
• Filtration


  • Takes place in the renal corpuscle
  • Glomerulus filters the blood and removes water and other substances
  • High pressured system. The blood is supplied by the afferent arterioles and removed by the efferent arterioles
  • GFR maintained by factors such as cardiac output, SNS tone, blood pressure, vascular volume
  • A feedback mechanism that keeps renal blood flow (RBF) and GFR constant despite changes in arterial blood pressure
• Reabsorption


  • Reabsorption occurs when filtered material is moved back into the blood, moves nutrients and water that has been filtered back into bloodstream
• Secretion


  • Secretion removes selected material from the blood and places it in the filtrate, waste products are secreted from the blood and form urine to be removed
• Categories of AKI


  • Prerenal
  • Intrarenal
  • Postrenal
• Cockcroft-Gault equation


  Used to estimate creatinine clearance, which is a measure of kidney function
• eGFR formula


  Used to estimate the glomerular filtration rate, which is a more accurate measure of kidney function
• Drugs constituting triple whammy

  • NSAIDs
  • ACE inhibitors
  • Diuretics
• Mechanism of renal damage from triple whammy

  Producing hypovolemia, and reduction of glomerular filtration rate and glomerular perfusion. Interferes with these compensatory mechanisms, and hence may produce renal failure
• Anaemia in kidney disease

  • Decrease in the production of erythropoietin (EPO) by the kidneys, leading to reduced red blood cell production in the bone marrow
  • Prior to commencing erythropoietin stimulating agents (ESA), trial of iron supplementation is recommended maintaining transferrin saturation (TSAT) >20% and ferritin between >100 μg/L
• Hyperkalaemia in kidney disease

  • The kidneys play a crucial role in potassium balance by excreting excess potassium into the urine
  • Remove drugs contributing, reducing potassium dietary intake, potassium wasting diuretics
• Renal bone disease


  • Characterized by abnormalities in calcium, phosphorus, parathyroid hormone (PTH), and vitamin D metabolism, leading to skeletal complications
  • Controlling serum phosphorus and PTH levels while maintaining adequate vitamin D levels. Dietary phosphorus restriction, phosphate binders, and dialysis are used to manage hyperphosphatemia
• Drugs excreted by the kidneys

  • Antibiotics: penicillins, cephalosporins, aminoglycosides, tetracycline
  • Beta blockers
  • Diuretics
  • Lithium
  • Digoxin
  • Procainamide
  • Cimetidine
  • Ranitidine
• GORD and PUD


  • Pregnancy, obesity, food and drinks and drugs that irritate mucosal lining (aspirin, NSAIDs, potassium chloride)
• Role of NSAIDs in PUD

  Inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX). By inhibiting COX, NSAIDs can reduce the production of these protective prostaglandins, making the stomach lining more vulnerable to damage from gastric acid
• Role of H. pylori in PUD

  Weakens protective mucous coating of the stomach and duodenum, acid and H Pylori irritate lining causing ulcer
• H. pylori eradication


  1. PPI (e.g. esomeprazole 20mg bd)

  2. Clarithromycin 500mg bd

  3. Amoxicillin 1g bd
• Adverse effects and mechanism of action of antacids, H2 receptor antagonists and proton pump inhibitors

  • Antacids neutralize stomach acid to relieve heartburn and indigestion, but can cause constipation or diarrhea
  • H2 receptor antagonists reduce stomach acid production and can lead to mild side effects like headache
  • Proton pump inhibitors block acid production more effectively, relieving symptoms and promoting ulcer healing, but long-term use may increase the risk of fractures and infections
• Management of GORD


  1. Elevate head of bed, avoid eating within 2-3 hours of bed, lose weight, stop smoking, reduce alcohol and modify diet

  2. Antacids – Mylanta (neutralise gastric acids)

  3. H2 receptors p famotidine (stop acid secretion)

  4. PPI – pantoprazole (stop acid secretion)
• Management of PUD


  1. Stop drug inducing PUD (NSAID)

  2. Misoprostol and Sucralfate (protective agent)

  3. Eradication of H. pylori

  4. Antacids – PPI, Clarithromycin, Amoxicillin