Week 2 - Liver disease Flashcards
What are the main functions of the liver
Liver is able to repair + regenerate new liver cells (hepatocytes)
FUNCTION:
1. Metabolism (drugs, bilirubin, protein, fat, etc.)
2. Clearance (drugs, bilirubin, toxins)
3. Produces bile
4. Synthesis (proteins, fibrinogen, cholesterol, clotting factors etc.)
5. Storage (of fat soluble vitamins + folic acid)
6. Homeostasis
7. Immunological
What are the common causes of liver disease (alcohol-related)
- Alcohol is most common cause for liver disease
- High alcohol intake (>14 units a week)
- approx. 50-70% cirrhosis is alcohol related
What are the common causes of liver disease (non-alcoholic fatty liver disease - NAFLD)
- Metabolic condition
- linked with CVD and diabetes
Other Causes:
- Viral hepatitis
- Infections
- Medicines + toxins
- Immune disease of the liver
- Inherited and metabolic disorders
- Cancer
- Biliary tract disorders
How is liver disease classified (time period - 2 types)
Classified according to time period it occurs over + pattern of the damage
Acute OR Chronic
- Acute
- rapid onset of symptoms which doesn’t exceed 6 months
- most common cause is medicines or viral hepatitis
- acute hepatitis is self-limiting (will recover)
- can develop into acute liver failure (ALF), acute liver dysfunction or chronic liver disease
SYMPTOMS: jaundice to encephalopath
= yellowing of eyes/ skin and + brain function affected i.e. confusion
- HYPERACUTE = symptoms last 0-7 days
- ACUTE = symptoms last 8-28 days
- SUBACUTE = symptoms last 29-84 days - Chronic
- symptoms last longer than 6 months
- most common cause alcohol or chronic viral hepatitis
- progressive + permanent structural damage
- patient is decompensated = can’t preform normal function
MANAGEMNET:
- treat underlying condition
- treat symptoms + complications
- liver transplant if needed
How is liver disease classified (pattern of damage - 2 types)
Classified according to time period it occurs over + pattern of the damage
Cholestatic or Hepatocellular
- Cholestatic / Cholestasis
- is disruption of bile flow (bile doest move in bile ducts) - Hepatocellular
- is injury to hepatocytes (liver cells)
- injury can be steatosis (fatty infiltration) and hepatitis (inflammation)
- injury can lead to fibrosis (liver scarring) + cirrhosis (permanent structural change to liver)
Fibrosis / Cirrhosis
- usually liver cells can repair themselves but ongoing damage to liver / hepatocytes = no repair = scarring develops (fibrosis) = blood flow is disrupted
- ongoing damage can cause cells to grow in wrong places = nodules form = cirrhosis
2 Types of cirrhosis
1. Compensated cirrhosis
- have enough hepatocytes for liver to carry out function
2. Decompenstated cirrhosis
- don’t have enough hepatocyte required for lover function (liver is extensively damaged)
What are the common signs and symptoms of liver disease
- Jaundice (yellowing of eyes, skin)
- buildup / high levels of bilirubin (>50) - Pale stools
- indicate biliary obstruction / bile excretion reduction (as binary is converted into faecal pigment when excreted) - Dark urine
- indicates obstruction
- conjugated bilirubin is excreted renally - Pruritus (itching)
- accumulation of bile under skin - Ascites
- swelling in abdomen (accumulation of / excess fluid) - Enchephalopathy
- changes in brain function e.g. confusion, coma - Varices + portal hypertension
- diabetes vessels due to increased portal vein pressure - Finger clubbing
- Red palms
- Spider nave (vascular changes)
- Bruising + bleeding
- Enlargement of male breast tissue
How is the severity of liver disease assessed (specifically for cirrhosis)
Assed by using “Child Pugh Scoring System”
- points are given for certain factors
Have 3 classes:
- Class A = <6 points
- have cirrhosis but fall into compensated category
- Class B = 7-9 points
- Class C = >10 points
- severe cirrhosis, fall into decompensated category need to consider medicine dose
List & explain the types of liver blood tests (5 Liver Function Tests ~ LFT)
Blood tests are used to assed liver function
- biochemical markers can be indicators that there is liver disease
- Bilirubin
- its a product of RBC breakdown
- when there’s liver damage bilirubin won’t be metabolised or excreted well = ↑ levels of bilirubin
- excreted via bile
- causes jaundice when levels >50 micromol/L
- bilirubin levels are ↑ by RBC breakdown, hepatocellular damage, cholestasis (disrupted bile flow) - Albumin
- a protein synthesised by liver
- albumin level ↓ in chronic liver disease (can’t be synthesised)
- ↓ albumin level causes oedema - Transaminases
- are enzyme in liver cells
- damaged liver cells release this enzyme = ↑ in levels
- not always present in liver damage, liver may be so damaged it doesn’t produce enzyme anymore
- transaminase levels ↑ in hepatitis, medicines, sepsis
- AST and ALT (ALT preferred as it is liver specific enzyme) - ALP and y-GT
Alkaline Phosphatase – ALP
- found in liver
- levels ↑ in cholestasis and damage to biliary tree
γ-Glutamyltransferase – GGT
- found in liver + biliary epithelial cells
- levels ↑ by enzyme inducers e.g. alcohol, medicined, cholestasis - PT/INR
PT = prothrombin time | INR = international normalised ratio
- clotting factors are synthesised by liver
- measuring clotting gives indication of how well liver is working
- levels ↑ if person has acute / chronic liver disease (as it should be synthesised quickly in healthy liver)
Explain how liver blood tests are used in practice
- If results are 2-3x above normal range = abnormal results
- At least 2 of the tests will be abnormal if have liver dysfunction
- Blood tests aren’t always abnormal in liver dysfunction e.g. transaminases
- Abnormal results aren’t always because of liver dysfunction
- Need to check medicines recommendation for hepatic impairment / function
- they may specific which liver blood test to monitor e.g. albumin or bilirubin
List other ways liver function can be assessed (NOT blood tests)
- Liver biopsy
- take samples of liver + examination pattern of damage - Imaging
- e.g. CT scan, MRI scan, liver ultrasound - Fibroscan
- assesses liver stiffness (the stiffer it is the more likely there is damage to liver)
- quick, non-invasive and not painful
List the complications that can occur from liver disease
- Ascites
- Hepatic encephalopathy
- Spontaneous bacterial peritonitis
- Portal hypertension and Varices
- Pruritus (itching)
How do you manage ascites (a complication)
- Diuretics
- help by shifting excess fluid from abdomen
- by inducing -ive fluid balance = amount of free fluid in abdomen is reduced
- e.g. Spironolactone (aldosterone inhibitor) = 1st line
- liver disease patients have ↑ aldosterone levels as liver can’t break it down (aldosterone causes H2o retention)
- e.g. Furosemide (loop diuretic)
- see effects through measuring weight daily (weight loss is related to fluid loss) - Fluid / Sodium Restriction
- fluid restriction - patient is more careful about amount of fluids consumed / avoid drinking too much
- given a set volume per day to prevent accumulation of excess fluid
- sodium restriction - reduce salt intake in diet
- salt leads to water retention = fluids buildup - Paracentesis
- draining fluid from stomach (if have large volume of ascites)
- used alongside diuretic
How do you manage hepatic encephalopathy (a complication)
Hepatic encephalopathy is acute confusion caused by changes in brain
- can cause confusion, mood changes, behavioural changed, coma
- drugs, infection, toxin accumulation (e.g. ammonia) can make this worse
TREATMENT:
1. Laxatives
- inhibit intestinal ammonia production by;
- changing pH of gut lumen (= ↓ ammonia absorption)
- ↓ colonic bacteria load = ↓ ammonia production
- AIM: increase bowel movement to ↓ ammonia levels through excretion
- e.g. lactulose liquid (1-3x daily)
2. Antibiotics
- kills naturally occurring gut bacteria (which produces ammonia) = ↓ ammonia levels
- e.g. Rifaxamin (550mg 2x daily)
3. L-ornithine L-aspartate Sachets
- amino acid supplements
- thes amino acids make body more efficient at removing ammonia
How do you manage spontaneous bacterial peritonitis (SBP - a complication)
SBP is a bacterial infection of the ascitic fluid
- causes severe pian, raised temp., raised WBC count
- usually caused by gram -ive but can be caused by gram +ive bacteria too
TREATMENT:
- Initially treat with broad spectrum IV antibiotics e.g. cephalosporins
- treat for 5 days then review
- If improved after 5 days can stop treatment, if not continue treatment
- For prevention can give oral antibiotics e.g. Norfloxacin / Ciprofloxacin
How do you manage portal hypertension and varices (a complication)
Portal hypertension caused by ↑ resistance to blood flow due to;
- compression of hepatic venues from regenerating nodules
Varices are weak blood vessels that form when pressure around liver builds up (from restricted blood flow)
- body produces new vessels to try reduce pressure
- new vessels may burst as they’re weak - variceal bleed (GI bleed)
MANAGEMENT of variceal bleed:
- May need resuscitation
- May need fluids, blood transfusion etc.
- Endoscopy (camera put inside to see if bleeding can be stopped)
- Give terlipressin (1-2mg) IV every 4-6 hours
- potent vasoconstrictor to try stop bleeding
- Give antibiotic (broad spectrum for 5 days)
- to prevent infection
- Give PPI
- to protect stomach
PREVENTION of 2nd bleed:
- Propranolol tablets (20-40mg, x2 daily)
- reduce pressure around liver
- B2 blocker and B1 blockers
