Week 7: Gastroenterology (3) (hepatology) Flashcards
1
Q
function of the liver
A
- 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
2
Q
anatomy of the liver
A
3
Q
Assessment of the patient with liver disease
A
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?
4
Q
chronic vs acute liver disease
A
Important to determine if acute liver injury/disease or chronic liver disease → if acute → look for evidence of acute liver failure
5
Q
Signs and symptoms of liver disease
A
- 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.
6
Q
Signs and symptoms of liver disease
A
- 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.
7
Q
stigmata of decompensated liver disease (4)
A
- Spider naevi
- encephalopathy (confusion)
- Palmar erythema
- Ascites
8
Q
liver screen
A
- 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
9
Q
invesrtigations of liver disease
A
- 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.
10
Q
The differential diagnosis of abnormal liver tests depends on the pattern of LFT abnormality and the level of abnormality.
A
- 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)
11
Q
what is in LFTs
A
albumin
ALT
AST
ALP
bilirubin
12
Q
Albumin
A
- synthetic function
- Can have renal cause too
- Decreased albumin= can be chronic liver disease
13
Q
- Damage to the liver causes an increase in enzyme release:
A
ALT
AST
14
Q
ALT
A
-
Alanine transaminase
- More specific to liver ‘L’
- Acute liver damage (likely for them both to go up)
15
Q
AST
A
-
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)
16
Q
ALP
A
-
alkaline phosphatase
- Bile ducts in the liver blocked (cholestasis)
- Can be high in children that are growing quickly/ also malignancy of bone
17
Q
what can be used to confirm ALP
A
gamma-GT
enzyme which will confirm if the raised ALP are caused by a damaged or obstructed bile duct as opposed to the bone
18
Q
bilirubin
A
-
Conjugated vs unconjugated
- Unconjugated
- Neonatal jaundice
- Unconjugated bilirubin can cross the BBB
- Damage to the brain
- Unconjugated
19
Q
LFT patterns in disease
A
20
Q
causes of chronic liver disease
A
-
Commonest causes
- Alcoholic liver disease
- Non-alcoholic steatohepatitis
- Viral hepatitis ( B and C)
-
Less common
- In women autoimmune hepatitis and primary biliary cholangitis (PBC)
- Men : primary sclerosing cholangitis which is associated with IBD
- Hemochromatosis
- Wilsons disease and anti LKM autoimmune hepatitis (adolescents)
21
Q
risk factors for chronic liver disease
A
- Blood transfusions prior to 1900
- IVDU
- operations
- sexual exposure
- medications
- FH liver disease, diabetes, IBD
- Obesity
- Alcohol
- Foreign travel
22
Q
Stigmata of chronic liver disease
A
- None
- Spider naevi
- Leukonychia
- Clubbing
- Dupuytren’s contracture
- Parotid swelling
- Testicular atrophy
- Loss of secondary sexual characteristics
- Gynaecomastia
- Loss of male distribution of hair
- Prominent superficial veins over abdomen
- Cachexia
- Mild splenomegally
- (Liver size irrelevant (can be large or small))
23
Q
presentations of chronic liver disease
A
- Asymptomatic with abnormal liver tests
- Tiredness
- Itch
- Arthralgia
- Jaundice
- Fluid retention (abdominal swelling)
- Upper GI bleed
- Confusion and drowsiness
24
Q
treatment of chronic liver disease
A
- Removing underlying aetiology (stopping drinking, weight loss, antivirals, venesection) to prevent further liver damage and progression to cirrhosis
- Maintain high protein diet
- treatment of acute presentation of chronic liver disease e.g. alcohol induced hepatitis - prednisolone
25
Q
cirrhosis
A
- End pathology of any cause of chronic liver disease
26
Q
causes of cirrhosis
A
- Alcohol
- Non-alcoholic fatty liver/ nonalcoholic steatohepatitis
- HBC, HCV
- Rarer: alpha-1-antitrypsin deficiency
- methotrexate
27
Q
suspect cirrhosis in any patient with chronic liver disease who has
A
- Thrombocytopenia
- Clinical stigmata of chronic liver disease
28
Q
investigations of cirrhosis
A
- Imaging
- Fibro scan
- Endoscopy (presence of varices)
29
Q
Signs of complications of cirrhosis
A
- Hypotension
- Oedema
- Ascites with shifting dullness
- Right sided pleural effusion (hepatic hydrothorax- transudate)
- Asterixis/flap
- Jaundice
30
Q
screening after cirrhosis diagnosis
A
- Should screen for varices in all patients with cirrhosis as primary prophylaxis can decrease risk of bleeding
- Osteoporosis risk- DEXA scan
- Hepatocellular carcinoma – can occur in patients with cirrhosis and patients should be screened using alpha fetoprotein and USS every 6 months (early diagnosis has a better prognosis)
31
Q
treatment of cirrhosis
A
- Ascites treatment- spironolactone or if tense, paracentesis
32
Q
spontaneous abcterial periotnitits)
A
33
Q
Hepatic encephalopathy
A
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.
34
Q
presentartion of hepatic encephalopathy
A
35
Q
Portal hypertension
A
- Build up of blood within the portal venous system (increased inflow and increased sinusoidal resistance)D
- Why?
- Due to cirrhosis
- Too much fibrotic tissue
- Not very expansive – needs to be because it drains the whole GI tract
- If its not very expansive veins entering the liver (from portal venous system) will be compressed
- Increase hydrostatic pressure within portal venous system
36
Q
Portal hypertension can cause
A
-
Ascites- fluid leakage into abdomen
- High hydrostatic pressure forcing water out
- Low albumin would also help this
- Build-up of pressure in splenic circulation- splenomegaly (need to feel for spleen and liver on exam)
-
Varices- blood can shunt from portal system to systemic circulation
- In normal life there are anastomoses between p. and s. system- not usually used
- If increase in venous pressure in portal system- blood shunts the other way
- Distention at site of anastomoses varices
- Varices can happen at the:
- Oesophagus
- Anal-rectal
- Umbilical
- Varices can happen at the:
- Distention at site of anastomoses varices
-
Hepatorenal syndrome
- Decreased kidney function causes failing liver
- Portal hypertension backlogs so badly that it affects the arterial blood supply (splanchnic) to the liver
- Causes splanchnic arterial vasodilation
- Perceived lack in circulation by the kidneys
- Actives RAAS- causes renal artery vasoconstriction- protects blood supply to kidney (however there is not problem with blood supply)
- Reduced perfusion of kidney reduced kidney function
37
Q
portal circulation
A
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
38
Q
oesophageal varcies
A
- 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
39
Q
Anal-rectal varices
A
- Between superior (which drain into the mesenteric vein) and middle and inferior rectal vein (internal iliac vein drains into IVC)
- Very rarely cause pain or bleed patients don’t usually present with these
40
Q
- Umbilical
A
- Ligamentum teres in adults- usually non functioning in adults
- Can become enlarged
- Caput medusae sign
41
Q
3 causes of jauncide
A
pre-hepatic
hepatic
post-hepatic
42
Q
pre-hepatic
A
- Too much break down of HB haem
- Haemaglobinopathies
- Sickle cell
- Thalamasemia
- Spherocytosis
- Haemolysis
- Too much demand for liver
- Liver cant conjugate it all
- Therefore some bilirubin is unconjugated
- Haemaglobinopathies
43
Q
hepatic
A
- Liver function down (reduced hepatocyte function)
- Reduced conjugating ability of the liver
- Causes
- Chronic liver disease
- Acute liver damage
44
Q
post hepatic
A
- Any obstructive condition to the bile duct if any part of excretion pathway is obstructed e.g. gall stones
- Most common
- Type of bilirubin likely to be raised is conjugated water soluble goes through blood stream to the kidney
- More bilirubin excreted by the kidney
- Therefore discolouration of the urine
- Dark urine, pale stools
45
Q
causes of post hepatic jaundice
A
- Gall stones
- Inflammation which causes scarring or narrowing of the biliary tree
- Enlargement of the head of the pancreas (pancreatic carcinoma) painless jaundice (red flag)
- Intrahepatic obstruction within the liver
- Inflammation/ oedema
- Tumour e.g. hepatocellular carcinoma (compression locally)
- Cirrhosis- no expansile
- Compresses veins – portal hypertension
- Also compresses bile ducts in liver
- Cirrhosis- no expansile
46
Q
hepaittis LFTs
A
ALT>500
- Hep A, B, C, E, CMV, EBV
- B, C chronic
- ALT levels usually peak before jaundice appears.
- Jaundice occurs in 70% Hep A, 35% acute Hep B, 25% Hep C
- Check for exposure
- Check HAV Ab IgM, HBc Ab IgM and HBsAg, Hep C IgG or Hep C RNA
