26784017
Description
Flashcards by Jenna Paterson, updated more than 1 year ago
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Created by Jenna Paterson
about 4 years ago
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| Question | Answer |
| Describe the breakdown of haemoglobin. | Breaks down to globin, iron and haem |
| Describe the breakdown and excretion of haem. | Breaks down to unconjugated bilirubin (insoluble) which is conjugated in the liver. Conjugated bilirubin is then excreted via biliary system and a smaller amount via the renal system. |
| What is jaundice? | = yellow discolouration (icterus) of the sclera or skin due to raised serum bilirubin. |
| What is pre-hepatic jaundice and its causes? | - An increase in RBC breakdown leading to an increase in unconjugated bilirubin. -Haemolysis - autoimmune, sickle cell disease, hereditary spherocytosis, thalassaemia, malaria, transfusion reaction - Extensive bruising/large haematoma |
| What is intrahepatic jaundice and its causes? | Failure to conjugate bilirubin in a damaged/inflamed liver or failure to excrete it into bile ducts --> unconjugated or conjugated hyperbilirubinemia - Decompensated chronic liver disease/cirrhosis (alcohol, NAFLD, viral, autoimmune, drugs, haemochromatosis, Wilsons, alpha-1-antitrypsin deficiency) - Acute liver injury/failure - acute viral (hep A, B, E), drug induced (paracetamol OD, acute alcoholic hepatitis, sepsis, ischaemia) - Drugs - nearly any can cause a rare drug induced liver injury (DILI) -Errors of bilirubin metabolism (e.g. Gilberts) |
| What is posthepatic jaundice and its causes? | Failure to remove conjugated bilirubin in bile via biliary system --> conjugated hyperbilirubinemia - Mechanical obstruction of large bile ducts: gallstones, cholangitis, cholangiocarcinoma, pancreatic mass, extrinsic compression - Drugs or pregnancy induced cholestasis (commonly Abx) - Autoimmune disease --> strictures (e.g. PBC, PSC) |
| How might someone with a pre-hepatic cause of jaundice present? | With jaundice and symptoms of anaemia (SOB, pre-syncope/syncope, exertional chest heaviness/pain, general tiredness/fatigue (most common) |
| How might someone with an intrahepatic cause of jaundice present? | Risk factors for chronic liver disease/cirrhosis (e.g. alcohol excess (ALD), obesity/T2DM (NAFLD), IVDU/tattoos/previous STI (viral hepatitis) or for acute liver injury/disease (paracetamol OD, generalised illness (hep A/E), acute alcohol binge (acute alcoholic hepatitis) Other symptoms of chronic liver disease/cirrhosis (e.g. worsening ascites, encephalopathy Recurrent on fasting/illness/stress but otherwise well- Gilbert's |
| How might someone with an post-hepatic cause of jaundice present? | - Pale stools/dark urine - Things specific to the cause e.g. RUQ pain, n&v - cholangitis, weight loss - malignancy, history of UC - PSC |
| What might painless jaundice indicate? | Most alarming is pancreatic malignancy - causes a post-hepatic obstructive jaundice |
| What are the causes of decompensated liver failure? | Acute renal failure Infection |
| Why might you do an ascitic tap? | Most importantly to rule out SBP Also can look for malignant cells Look at protein levels to understand why there is ascites |
| What is the first line imaging investigation for someone with liver dysfunction? | Abdominal US |
| What ECG finding can cirrhosis cause? | Prolonged QTc |
| Why might you measure somebody's ceruloplasmin? What other test might you do? | To rule out Wilson's disease. Serum copper |
| What does a positive AMA indicate? | Anti-mitochondrial Ab Can indicate PBC |
| What does a positive ASMA and/or ANA indicate? | ASMA - anti-smooth muscle Ab ANA - anti nuclear Ab Autoimmune hepatitis |
| Why are iron studies important in liver disease? | Rule out haemochromatosis |
| Why might platelets be low in liver disease? | Low platelets often seen with portal HTN in cirrhosis causing splenomegaly and platelet sequestration |
| What are the stages of hepatic encephalopathy? | - I - mild confusion, agitation, irritability, sleep disturbance, decreased attention - II - lethargy, disorientation, inappropriate behaviour, drowsiness - III - somnolent but arousable, slurred speech, confused, aggressive V - coma |
| What is the SAAG? | The serum-ascites albumin gradient (SAAG) can be used to differentiate ascites from portal HTN and other causes. |
| What are the causes of a high SAAG and the cut-off for this? | SAAG > 11 = a transudate. This suggests the presence of portal HTN, which may be caused by: ○ Liver cirrhosis ○ Hepatic failure ○ Alcoholic hepatitis ○ Fulminant hepatic failure ○ Liver metastases ○ Venous occlusion ○ Cardiac ascites |
| What are the causes of a low SAAG and the cut-off for this? | SAAG <11 = an exudate ○ Infection ○ Malignancy ○ Pancreatitis ○ Nephrotic syndrome |
| How is ascites managed? | Daily fluid balance Daily weights Dietician review - advice low salt diet If renal function satisfactory and potassium normal then start spironolactone 100mg daily and titrate with close monitoring of renal function. If WCC >500mm3 or neutrophils >250mm3 then treat as SBP with broad spectrum Abx. If causing severe discomfort/respiratory compromise or hasn't responded to the above then large volume paracentesis can be performed. |
| What is large volume paracentesis and what should be given alongside this procedure? | - Ascitic drain into the abdomen to drain the ascites. - Drain should be removed within 6 hours to reduce infection risk - 20% of albumin solution is given IV for every 2.5L of ascites drained |
| Why are people with liver disease at an increased risk of bleeding? | - Prolonged INR; secondary to failing synthetic liver function - Low platelets; portal HTN results in splenomegaly and platelet sequestration - Portal HTN secondary to cirrhosis; causes oesophageal and gastric varices which increase the risk of upper GI bleed - Alcoholic liver disease; bleeding ulcers and gastritis which may lead to an upper GI bleed |
| How is bleeding in liver disease managed? | - Vitamin K - ensures levels are replete - Withhold anticoags/NSAIDs - Discuss with haematologist if coagulopathic and bleeding and screen for DIC - If upper GI bleed suspected then needs urgent endoscopy - Discuss with senior immediately - may need to be moved to HDU for invasive monitoring and terlipressin - Antibiotics - reduced mortality from GI bleeding in patients with cirrhosis |
| By which mode of inheritance is hereditary haemochromatosis passed onto offspring? | Autosomal recessive for types 1,2,3 Autosomal dominant for type 4 (less common) |
| What is the pathophysiology of hereditary haemochromatosis? | Associated with a defect in the iron regulating hormone hepcidin --> increased intestinal absorption of iron and subsequent deposition in the liver, pancreas, heart, joints, skin and pituitary. |
| How does hereditary haemochromatosis present? | Classic triad of fatigue, arthralgia and sexual dysfunction. May also present with complications. |
| What are the complications of hereditary haemochromatosis? | ○ Liver cirrhosis ○ Type 1 diabetes ○ Skin discolouration ○ Dilated cardiomyopathy ○ Arthropathy ○ Hypogonadism ○ HCC |
| How can hereditary haemochromatosis be diagnosed? | - Serum transferrin saturation is the best initial screening test - >45% suggests haemochromatosis - Raised serum ferritin is also seen - but this is non-specific as acute phase protein. - HFE gene testing for mutations - Liver biopsy/fibroscan can assess liver fibrosis - can see iron deposition on histology. - MRI scans can demonstrate iron overload. |
| How should someone with hereditary haemochromatosis be managed? | - MDT approach - Avoid alcohol and iron supplementation in their diet - Aim for a healthy BMI to reduce fat-related liver inflam - Regular venesection to reduce iron stores - May require chelation with desferrioxamine - Liver transplantation in end stage cirrhosis - Patients with haemochromatosis and known cirrhosis should undergo annual abdominal US and AFP testing as at risk of hepatocellular carcinoma. |
| What is the diagnostic criteria for SBP? | Neutrophils >250 or total WCC > 500 in ascitic tap |
| How is SBP treated? | - Abx - IV co-amoxiclav - IV infusion salt poor albumin (100ml 20% albumin): 1.5g/kg day 1, 1g/kg day 3 - Long term prophylaxis needed with co-trimoxazole or rifaximin |
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