Alcoholic Liver Disease Flashcards
What are the main functions of the liver?
Bile production= aids in absorption of fat + certain vitamins
Fat-soluble vitamin storage + metabolism (A,D,B, K)
Drug metabolism
Plasma protein synthesis i.e. albumin/globulin/protein C/protein S/ clotting factors in intrinsic and extrinsic pathway
Immune response
Bilirubin metabolism
Thyroid hormone function by deiodination of T4->T3
Glycogen storage + gluconeogenesis
Blood detoxification
Iron store
Processes cholesterol
What conditions are included under ALD?
Alcoholic fatty liver +/- hepatitis
Alcoholic hepatitis
Cirrhosis
Chronic liver disease (alcoholism is the moat common cause)
What is the pathophysiology of liver cirrhosis due to chronic alcohol abuse?
Chronically high intake of alcohol leads to chronic liver injury:
-inflammation due to alcohol making gut leaky which leads to bacteria entering blood and activating the Kupffer cells
- matrix deposition- oxidative stress causes stellate cell activation i.e. leads to fibrosis
- necrosis
- angiogenesis
- malnutrition leads to impaired regeneration of tissue
I.e. progressive matrix deposition and scar formation leads to fibrosis formation
What are the clinical signs of liver cirrhosis?
Leuconychia= white nails -> sign of hypoalbuminaemia
Clubbing
Palmar erythema (effects of oestrogen)
Hyperdynamic circulation= abnormal increased circulating volume
I.e. either presents with collapsing pulse or with bounding pulse
Dupuytrens contracture
Spider naevi
Xanthelasma
Gynaecomastia (effects of oestrogen)
Loss of body hair (look in axilla)-> effects of oestrogen
Hepatomegaly (NOTE: small liver seen in late disease)
Ascites (portal HTN)
Caput Medusa
Splenomegaly (due to increased pressure across the portal venous system)
What signs occur in liver cirrhosis in association with oestrogen and why do they occur?
Gynacomastia
Loss of axilla hair
Palmar erythema
Increased production of androstenedione by adrenal glands
Increased aromatisation of androstenedione to oestrogen
Loss of clearance of adrenal androgens by liver
Decreased oestrogen break down by the liver
What are the main complications associated with liver cirrhosis and what are the signs of each?
Hepatic failure
- coagulopathy due to loss of clotting factor sythesis= easy bruising
- encephalopathy (due to rise in ammonia)= liver flap
- hypoalbuminaemia -> oedema
- sepsis
- hypoglycaemia
Portal hypertension
- Ascites
- splenomegaly
- oesophageal varices
- portosystemic shunt
- Caput medusa
Why does portal hypertension occur in liver cirrhosis and how can it be managed?
Liver cirrhosis causes obstruction to portal blood flow through the liver which increases the pressure in the hepatic portal system
Beta-blockers= propranolol
-splanchnic vasoconstriction to cause decreases portal and collateral blood flow which decreases portal hypertension
Portosystemic shunts= Transjugular intrahepatic portosystemic shunts
-metal stent guided to intrahepatic branch of portal vein via the internal jugular vein to enable side-to-side shunt
I.e. portal system bypasses the liver and goes straight input systemic circ
What LFT changes are indicative of liver cirrohsis?
Normal or raised bilirubin Raised AST and ALT Raised gamma GT Decreased albumin Raised PT/INR
What imaging techniques can be used in liver cirrhosis?
Liver ultrasound + duplex
- hepatomegaly or small liver depending on liver stage
- splenomegaly
- focal liver lesions
- reverse flow in hepatic vein
MRI
- right posterior hepatic notch= more frequent in alcoholic cirrhosis
- increased caudate lobe size
Why does ascites occur in liver cirrhosis? (3 main mechanisms)
NO, ANP and prostaglandins released in association with liver cirrhosis leads to peripheral vasodilation which decreases effective BV and triggers RAAS
I.e. leads to SALT + WATER RETENTION
PORTAL HYDROSTATIC PRESSURE leads to increased fluid accumulation in peritoneal cavity due to increase hepatic and splanchnic lymph production
LOW SERUM ALBUMIN reduces plasma oncotic pressure which contributes to increased driving force of water out of portal veins
What is the main aim of ascites management? What is the maximum amount of fluid which can be moved in this way?
Reduce sodium intake and increase renal sodium excretion= leads to net fluid reabsorption
Reabsorption= 500-700 ml in 24 hrs
What are the methods of ascites management?
Fluid restriction <1.5L/day
Low-salt diet= 40-100 mmol/d
Spironolactone= 100mg/24hr
NOTE: furosemide can be used if response to spironolactone is poor
Paracentesis= tense ascites or when diuresis not sufficient in meeting fluid targets
Shunts (TIPS)
-when ascites resistant to other methods of treatment
I.e. decreasing portal hypertension can lead to decrease in ascites
What does patient need to be monitored for when places on furosemide for ascites?
Hyponatraemia
Hypokalaemia
Hypovolaemia
A patient suffering from ascites is put onto spironolactone. A recent blood results shows raised creatinine. What has happened?
Over-diuresis and hypovolaemia
What condition can patients present with before it progresses to liver cirrhosis? How does a patient present?
Alcoholic hepatitis
Raised temp, pulse and resp (TPR) D+V Tender hepatomegaly Jaundice Ascites
What are signs of severe alcoholic hepatitis?
Jaundice
Encephalopathy
Coagulopathy
What are the consequences of decreased oestrogen breakdown in liver disease?
Palmar erythema Spider Naevi Gynaecomastia Loss of body hair Testicular atrophy
Why are oesophageal varices associated with liver cirrhosis? What signs are associated with oesophageal varices?
The increased portal hypertension leads to increased pressure in the veins of the oesophagus which leads to them dilating and forming varices.
Signs:
- haematemesis= coffee-ground vomit
- melena- black tarry stool
- collapse
- anaemia
- abdo pain
If patient has been admitted for ALD then they will experience alcohol withdrawal secondary to admission. What are the signs ? How can alcohol withdrawal be managed?
Signs:
- increase pulse
- decreased BP
- tremor
- fits
- hallucinations
Management:
-use CIWA- Ar to score patient on withdrawal symptoms and inform management
-1st 3 days= chlordiazepoxide (10-50mg/6h)
-IV high dose B1
NOTE: need to plan weaning regime over 5-7days
I.e. sedative and hypnotic medication in benzos class
What are the possible cause of chronic liver disease?
Alcoholic liver disease
Non-alcoholic fatty liver disease
Cirrhosis
What is the progression of hepatic injury due to chronic excessive alcohol consumption?
Develop alcoholic fatty liver
-alcohol metabolism leads to fat deposition in liver which causes cells to become swollen with fat but not damaged i.e. steatosis
Alcoholic hepatitis
-prolonged period of inflammation
Alcoholic cirrhosis= final stages of ALD
-scar tissue formation due to matrix deposition
What would the bloods of someone with ALD show?
Raised MCV= due to alcohol suppressing bone marrow function leading to production of large immature RBC
Elevated ALT + AST + GGT
Low albumin
Increased PT/INR = clotting factors effected
What scans can be done for ALD?
USS= can show fatty liver i.e. echogenicity
- can do “fibroscan” as part of USS to assess for cirrhosis by sending through high frequency waves
How can ALD be managed?
CONSERVATIVE:
-Encourage alcohol cessation= need to stop completely
Eg can refer to alcohol specialist nurse
-Nutritional support:
-Thiamine (B1)especially to prevent
Wenricke-Korsaffs syndrome as complication
E.g. Pabrinex= B1 replacement (alcohol prevents B1 absorption)
- Steroids can be used for alcoholic hepatitis
- Treat complications= portal hypertension, oesophageal varices, ascites, anaemia (associated with alcohol)
Refer to liver transplant (must be 3 months clear of any alcohol consumption)
How does the presentation of alcohol withdrawal change depending on time since last drink?
6-12hrs= tremors, sweating, cravings, headache, anxiety 12-24hrs= hallucinations 24-48hrs= seizures 48-72hrs= delirium tremens
Why does alcohol withdrawal lead to delirium tremens?
With alcohol:
- GABA receptors stimulated
- glutamate receptors inhibited
With chronic alcohol use:
-body compensates for chronically high alcohol levels by down regulating GABA receptors and up-regulating glutamate receptors
Withdrawal of alcohol:
-GABA underfunction and glutamate over functions leading to excessive excitatory activity
I.e. acute confusion, severe agitation, tachycardia, hypertension, tremor, ataxia, arrythmias
What is Wenricke-Korsakoff syndrome and what are the 2 different stages? How can it be prevented?
Occurs with alcohol excess due to decreased absorption or intake of vitamin B1/thiamine
Wenrickes encephalopathy = medical emergency
- confusion
- oculomotor disturbances
- ataxia
Korsakoff-syndrome = damage to mammillary bodies
- retrograde and antegrade memory loss
- behavioural changes
Pabrinex (B1 replacement)
Alcohol can severely impact the gut. What other conditions are people with high intact of alcohol at risk of developing?
Gastritis
Pancreatitis
Ulcers
GORD
Malnutrition
Anaemia
Oesophageal cancers
