Week 7: Gastroenterology (3) (hepatology) Flashcards
function of the liver
- Function
- Nutrition/metabolic
- Stores glycogen
- Releases glucoses
- Absorbs fats, fat soluble vitamins and iron
- Manufactures cholesterol
- Bile salts
- Dissolves dietary fats (detergent)
- Bilirubin
- Breakdown product of haemoglobin
- Clotting factors
- Manufactures most clotting products
- Detoxification
- Drug excretion
- Alcohol breakdown
- Immune function
- Kupfer cells engulf antigens (bacteria)
- Manufactures proteins
- Albumin
- Binding proteins
- Nutrition/metabolic
anatomy of the liver
Assessment of the patient with liver disease
When taking a history from a patient with liver disease it is important to ask about risk factors:
- Blood transfusions prior to 1990 in UK.
- IVDU.
- Operations / vaccination with dubious sterile procedures.
- Sexual exposure.
- Medications (prescribed / self prescribed).
- FH of liver disease, Diabetes, IBD
- Obesity and other features of metabolic syndrome.
- Alcohol (?dependent).
- Foreign travel?
chronic vs acute liver disease
Important to determine if acute liver injury/disease or chronic liver disease → if acute → look for evidence of acute liver failure
Signs and symptoms of liver disease
- Skin and eyes that appear yellowish (jaundice)
- Abdominal pain and swelling.
- Swelling in the legs and ankles.
- Itchy skin.
- Dark urine color.
- Pale stool color.
- Chronic fatigue.
- Nausea or vomiting.
Signs and symptoms of liver disease
- Skin and eyes that appear yellowish (jaundice)
- Abdominal pain and swelling.
- Swelling in the legs and ankles.
- Itchy skin.
- Dark urine color.
- Pale stool color.
- Chronic fatigue.
- Nausea or vomiting.
stigmata of decompensated liver disease (4)
- Spider naevi
- encephalopathy (confusion)
- Palmar erythema
- Ascites
liver screen
- Hepatitis B&C Serology (in acute liver disease consider Hep A & E if marked ALT rise)
- Iron studies (Ferritin & transferrin saturation)
- Autoantibodies (AMA & SMA) and immunoglobulins
- Consider caeuruloplasmin if age under 30 years
- Alpha-a-antitrypsin
- Coeliac serology
- TFTs, lipids & glucose
invesrtigations of liver disease
- Thrombocytopenia is a sensitive marker of liver fibrosis
- LFTs should give you an idea of where the damage is occurring; the hepatocytes (ALT rise) or the ducts (ALP rise; a concurrent rise in gamma GT can be helpful to confirm that the ALP is liver in origin).
- The Bilirubin, Albumin and Prothrombin time (or INR) are all markers of synthetic function, and in acute liver disease abnormalities in synthetic function should raise concern.
The differential diagnosis of abnormal liver tests depends on the pattern of LFT abnormality and the level of abnormality.
- If the LFTs suggest a cholestatic abnormality the first test should be an ultrasound to assess if the ducts are dilated (obstructive jaundice) or not.
- There may also be USS findings that suggest cirrhosis (coarse texture, nodularity, splenomegaly or ascites)
what is in LFTs
albumin
ALT
AST
ALP
bilirubin
Albumin
- synthetic function
- Can have renal cause too
- Decreased albumin= can be chronic liver disease
- Damage to the liver causes an increase in enzyme release:
ALT
AST
ALT
-
Alanine transaminase
- More specific to liver ‘L’
- Acute liver damage (likely for them both to go up)
AST
-
Aspartate transaminase
- Also found in cardiac (increased troponin) and skeletal muscle (look at increase in CK) and RBC (FBC)
- Chronic liver damage (likely for them both to go up)
ALP
-
alkaline phosphatase
- Bile ducts in the liver blocked (cholestasis)
- Can be high in children that are growing quickly/ also malignancy of bone
what can be used to confirm ALP
gamma-GT
enzyme which will confirm if the raised ALP are caused by a damaged or obstructed bile duct as opposed to the bone
bilirubin
-
Conjugated vs unconjugated
- Unconjugated
- Neonatal jaundice
- Unconjugated bilirubin can cross the BBB
- Damage to the brain
- Unconjugated
LFT patterns in disease
spontaneous abcterial periotnitits)
Hepatic encephalopathy
Hepatic encephalopathy is a nervous system disorder brought on by severe liver disease. When the liver doesn’t work properly, toxins (ammonia) build up in the blood. These toxins can travel to the brain and affect brain function. People with hepatic encephalopathy may seem confused.
presentartion of hepatic encephalopathy
portal circulation
Portal circulation- the network of veins that drains via the liver into the inferior vena cava
- Three main veins that comprise the portal system:
- Inferior mesenteric vein
- Drains the descending colon
- Superior mesenteric vein
- Drains the ascending colon and other midgut structures
- Splenic vein
- Inferior mesenteric vein drains into splenic vein and join with the superior mesenteric vein to form the portal vein
- Inferior mesenteric vein
- Portal vein enters the liver and drains it, then forms the hepatic veins which drain into the inferior vena cava
oesophageal varcies
- Upper 2/3 drains into oesophageal veins- goes through the azygous drains into the superior vena cava
- Distal portion drains into the left gastric vein- drains into the portal vein
- At the junction where there are veins draining into the main systemic circulation (SVC) is where the pressure builds up.
- Veins are superficial- therefore become dilated easy to rupture
- Significant Haematemesis
