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Med 2 > Alcoholic Liver Disease > Flashcards

Alcoholic Liver Disease Flashcards

1
Q

Define alcoholic liver disease

A

Manifestations of alcohol overconsumption - leading to indlammation and scarring of the liver tissue due to progressive destrucation and regeneration of liver parenchyma.

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2
Q

What are the different subtypes on the spectrum of alcoholic liver disease?

A

Alcoholic fatty liver disease
Alcoholic hepatitis
Cirrhosis

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3
Q

What is the relevant epidemiology of alcoholic liver disease?

A

Peak incidence in 40-50yrs
Twice as common in males
Note is less common than non-alcoholic liver fatty liver disease

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4
Q

What are some risk factors for alcoholic liver disease?

A

Alcohol consumption - chronic and excessive
Genetic predisposition - polymorphism in alcohol metabolism enzymes (alcohol dehydrogenase and aldehyde dehydrogenase)
Nutritional status: malnutrion exacerbates due to reduced hepatocyte regen and impaired immune response
Co-existing liver conditions - chronic viral hepatitis (particularly C)

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5
Q

What are the key clinical features of early-stage alcoholic liver disease?

A

Asymptomatic or non-specific
Fatigue
Malaise
Abdominal pain
Anorexia
Weakness
Nausea / Vomiting

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6
Q

What are the signs of alcoholic hepatitis?

A

Jaundice (common)
RUQ pain (common
Hepatomegaly (common) - enlarged and smooth edge but rarely tender to palpation
Palmar erythema
Peripheral oedema
Clubbing
Dupuytren’s contracture
Pruritis
Xanthomas
Spider angiomas

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7
Q

What are the signs of a raised estrogen level in alcoholic liver disease?

A

Gynaecomastia and testicular atrophy (males)
Amenorrhoea (females)
Loss of libido
Loss of body hair

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8
Q

What are the signs/symptoms of portal hypertension as a result of alcoholic cirrhosis?

A

Ascites
Dilated veins (caput medusae)
Variceal bleeding and haemorrhage
Splenomegaly

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9
Q

What first line investigations should be done for alcoholic liver disease?

A

Bloods - LFts, FBCs, clotting studies, serum electrolytes
Alcohol consumption questionnaires - AUDIT to help quantify alcohol intake and harmful behaviour patterns.

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10
Q

What may LFT results show in alcoholic liver disease?

A

Raised GGT
Raised AST
AST:ALT ratio greater than 2:1 (greater than 3:1 indicates acute)
AST - typically 100-2000IU
Mild elevation in bilirubin and decreased albumin

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11
Q

What are the second line investigations that may be done in alcoholic liver disease?

A

Imaging - US abdo - liver size, exhotexture, rule out malignancy/gallstones, cirrhosis or portal hypertension
Liver biopsy - if concurrent liver disease suspected.

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12
Q

What are some common complications of alcoholic liver disease?

A
  1. Hepatic encephalopathy
  2. Portal hypertension (from cirrhosis) - secondary variceal haemorrhage
  3. Ascites complications by spontaneous bacterial peritonitis.
  4. Hepato-renal syndrome - can lead to acute kidney failure due to widespread splanchnic vasodilation
  5. Hepatocellular carcinoma - hepatic ultrasound every 6m or 1yr to screen
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13
Q

Give an overview of hepatic encephalopathy

A

Reduced ability of liver to metabolise ammonia and neurotoxins.
Collateral vessels allow to bypass the liver.
Build up of ammonia can cause encephalopathy
Signs and symptoms - confusion, drowsiness, hyperventilation, asterixis, fetor hepaticus, reduced consciousness

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14
Q

What are the key differential diagnosis for alcoholic liver disease?

A
  1. Non-alcoholic liver disease - more strongly associated with obesity, T2DM, hyperlipidemia and HTN
  2. Viral hepatitis - serological markers, drug use, unsafe sexual practices
  3. Autoimmune hepatitis - autoantibodies (ANA, SMA, LKM1), elevated IgG
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15
Q

What are the general measures that should be taken to treat alcoholic liver disease?

A

Alcohol abstinence - biggest prognostic factor
Weight loss - if overweight or obese may also have NAFLD
Vaccination - hep A and Hep B
Nutrition - high protein (1-1.5g per kg), may need NGT

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16
Q

What is the treatment for alcoholic withdrawal?

A

Benzodiazepines - diazepam
If seizures or delirium tremens - lorazepam is first line and taken orally.

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17
Q

What is the typical treatment plan for acute alcoholic hepatitis?

A

Glucorticoids (prednisolone)
Improve short term survival but have limited long term benefit.
Use Maddreys discriminant function -> identify severe acute alcoholic hepatitis in scores of 32+ -> these require biopsy.
Pnetoxifylline can be used as an alternative to glucorticoids.

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18
Q

How does hepatic encephalopathy tend to present?

A

Confusion
Drowsiness
Hyperventilation
Asterixis
Fetor hepaticus

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19
Q

What medication is given for alcohol withdrawal under the CIWA score?

A

Oral chlordiazepoxide (benzo) for agitation and anxiety
Lorazepam IV (delirium tremens/seizure)
Haloperidol IM (anti-psychotic)
Pabrinx IV followed by oral thiamine - to prevent encephalopathy.

Given PRN based on CIWA score

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20
Q

How is the CIWA score interpreted for alcohol withdrawal medication?

A

Score 8> monitor hourly and administer PRN meds, 1hr for 8hrs than 2hrs if stable then 4hrs if stable.
Score <8 monitor 4hrly for 72hrs then discontinue is score remains <8.

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21
Q

What are the acute causes of liver failure?

A

Paracetamol overdose
Alcohol
Viral hepatitis
Acute fatty liver of pregnancy.

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22
Q

What are the key clinical features of acute liver failure?

A

Jaundice
Coagulopathy - raised prothrombin time
Hypoalbuminaemia
Hepatic encephalopathy
Renal failure (hepatorenal syndrome).

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23
Q

What are the different lobes of the liver?

A

Right
Left
Caudate
Quadrate

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24
Q

What are the key ligaments of the liver?

A

Coronary ligament
The left and right triangular ligament (from unification of the anterior and posterior coronary ligaments)
The falciform ligament (anterior surface)
The round ligament (free edge of falciform - remnant of paraumbilical veins)
The ligamentum venosum (post/inferior surface - remnant of ductus venosus).

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25
Q

What makes up the dual blood supply to the liver?

A

Hepatic artery proper (25%) - oxygenated blood for non-parenchymal structures
Hepatic portal vein 75% - partially oxygenated, nutrient-rich from the small intestine, allows performing gut related function e.g detox.

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26
Q

What is the venous drainage of the liver?

A

Hepatic veins -> IVC -> right atrium.

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27
Q

What are the key functions of the liver?

A

Production = bile, plasma, clotting factors, gluconeogenesis
Storage = fat-soluble vitamins (ADEK), glycogen, copper, iron and B12
Metabolism = drugs, toxins and bilirubin
Immune response = phagocytosis
De-ionisation of T4 to T3.

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28
Q

What is the role of the liver in coagulation?

A

All clotting factors are synthesised in the liver (except for VIII)
Protein C and Portein S prevent hypercoagulation

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29
Q

How is coagulation affected in liver disease?

A

GLobal decline in clotting factors -> affecting intrinsic and extrinsic pathways.
Thrombocytopaenia -> secondary to hypersplenism caused by portal hypertension -> increased platelet sequestration and destruction.

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30
Q

What is the metabolism of bilirubin?

A
  1. Hemolysis produces unconjugated bilirubin
  2. Bounds to albumin = conjugated bilirubin
  3. Metabolised by hepatocytes and secreted via biliary tract into small intestine as bile
  4. Metabolised by bacterial proteases into urobilinogen
  5. May continue and be metabolised to sterobilin in faeces
  6. May be reasbobred and recycled through hepatocytes repeating step 3+
  7. May be reabsorbed and metabolised in kidneys to urobilin secreted in urine.
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31
Q

In LFTs what are key markers of hepatocellular injury?

A

AST (aspartate aminotransferase)
ALT (alanine aminotransferase)
As enzymes found within hepatocytes
Key disease: hepatitis, cirrhosis

32
Q

What is the key LFT result seen in alcoholic-related liver disease?

A

AST:ALT ration >2:1

33
Q

What is ALP a key diagnostic indicator for?

A

Found in biliary epithelial cell and bones
Raised in cholestasis or bone disease

34
Q

What is GGT a key diagnostic marker for?

A

Found in hepatocytes and biliary epithelial cells
Non specific but highly sensitive for liver damage and cholestasis

35
Q

How can ALP and GGT be interpreted together?

A

Raised ALP with normal GGT suggests bone disease
Raised ALP with raised GGT is more suggestive of cholestasis
Isolated raised GGT is classically associated with alcohol excess.

36
Q

What are the different types of jaundice?

A

Excess production = pre-hepatic = haemolysis
Breakdown in metabolism = hepatocellular jaundice
Blockage in bile excreation = intra/extrahepatic obstruction known as cholestatic jaundice.

37
Q

What tests can indicate liver synthetic function?

A

Albumin
Coagulation screen

38
Q

What are the roles of albumin in the body?

A

Binds water, cations, fatty acids and bilirubin
Maintains the oncotic pressure of blood

39
Q

What are the common causes of low albumin?

A

Less production (malnutrition, severe liver disease)
Increased loss (protein-losing enteropathies, nephrotic syndrome).

40
Q

How can ALT and ALP be used together for diagnostic purposes?

A

x10 inc ALT and less than 3x in ALP = predominant hepatocellular
Less than x10 inc ALT and more than x3 inc ALP is predominantly cholestasis.
Can be mixed.

41
Q

What is the use of different imaging techniques for the liver?

A

US = biliary tree or structural lesions
Elastography = US to measure stiffness of liver
Tripe-phase CT/MRI = high sensitive liver lesions.
MRCP = biliary and pancreatic ducts
ERCP = treatment of biliary and pancreatic ducts.

42
Q

How can ultrasound and what techniques be used to differentiated between different stages of liver disease?

A
  1. Fatty liver = increased attenuation
  2. Inflammation and fibrosis = shear wave dispersion increased
  3. Shear wave elastography - shows roughened texture often seen in fibrosis and cirrhosis
  4. CHI quantification for liver cancer.
43
Q

What bloods are included in a liver screen?

A

Hepatitis serology A/B/C
EPV
Cytomegalocirus
AMA
ASMA
Anti-liver/kideny microsomial antibodies
ANA
p-ANA
IgM and IgG
Alpha-1-antitrypsin
Serum copper and caeruloplasmin
Ferritin

44
Q

What is the key process of non-alcoholic fatty liver disease?

A

Excessive fat (esp. triglycerides) in the liver cells
Associated with metabolic syndrome - insulin resistance, obesity and T2DM.

45
Q

What are the key investigations for NAFLD?

A

Increased ALT
US-liver/FibroScan
ELF blood test
Liver biopsy

46
Q

What scoring systems can be used for NAFLD?

A

NAFLD fibrosis score - indicates likelihood of advanced liver disease
FIB-4 score - indicates extent of fibrosis, suggest if biopsy is needed.

47
Q

What are the key features of alcohol-related fatty liver disease?

A

Severe inflammation of the liver related to excess alcohol consumption
Characterised by rapid-onset jaundice, malaise and tender hepatomegaly

48
Q

What are the three stages of ARFLD?

A
  1. Alcoholic fatty liver (hepatic steatosis) - reversible with abstinence
  2. Alcoholic hepatitis (inflammation) - mild changes are reversible
  3. Cirrhosis (scarring) - irreversible but abstinence prevents more damage
49
Q

What are the key investigations for ARFLD?

A

Bedside: US-liver/fibroscan
Bloods: Inc MCV, Inc ALT+AST (ratio >1.5), Inc GGT inc ALP in later disease, inc bilirubin in cirrhosis,
dec albumin, inc PT
Imaging: Endoscopy (oesophageal varices), CT/MRI scans, liver biospy.

50
Q

What is hepatitis B?
Why does it lead to cirrhosis?

A

Double-stranded DNA virus
Direct contact with bodily fluids + vertical transmission
Most recover within 1-3 months however 5-15% become chronic carriers
15% chronic HBV infection develop cirrhosis within 5 years.
More common in developing world.

51
Q

What is hepatitis C?
How often does it lead to cirrhosis?

A

RNA virus
Spread by blood and bodily fluids
No vaccine available
Curable 90% of cases with direct acting anti-virals
1 in 4 make a full recovery
3 in 4 develop chronic disease with risk of cirrhosis.

52
Q

What are the most common causes of liver cirrhosis?

A

ALD
NAFLD
Hepatitis B
Hepatitis C

53
Q

What is the basic idea of liver cirrhosis?

A

End stage of chronic inflammation and damage to liver cells
Funcational cells are replaced with nodules of scar tissue (fibrosis)
This affects the structure and blood flow in the liver.
Increased resistance in the portal system = portal hypertension.

54
Q

What are some rarer causes of liver cirrhosis?

A

Autoimmune hepatitis
Primary biliary cholangitis.
A1ATD
CF
Haemochromatosis - iron overload
Wilsons disease - inc copper.
Drugs (amiodarone, methotrexate and valproate)

55
Q

What is compensated cirrhosis?

A

Liver maintaining important functions despite disease

56
Q

What is decompensated cirrhosis?

A

Acute deterioration in liver function in a patient with cirrhosis
High mortality, characterised by jaundice, ascities, hepatic encephalopathy, hepato-renal syndrome or variceal bleeding.
May consider liver transplant.

57
Q

What key investigations are done for a decompensated liver cirrhosis patient?

A

Bedside: NEWS and glucose
Bloods: FBC, LFT, Coag, Gluc, Ca/Po4/Mg, blood cultures, CRP
Urine Dip
CXR
Request USS abdo
Ascitis tap
Record recent daily alcohol intake.

58
Q

What is an important marker for liver cancer?

A

Alpha-fetoprotein.

59
Q

What scoring systems are important in liver cirrhosis?

A

MELD
Child-Pugh

60
Q

What is the purpose of the MELD scoring system?

A

Calculates risk of 3 month mortality for cirrhosis to help prioritise for liver transplant planning

Consideres: Age, creatinine, bilirubin, INR, sodium, Albumin

61
Q

What is the purpose of the Child-Pugh scoring system?

A

Calculate the severity /prognosis of cirrhosis.

Considers: Bilirubin, albumin, INR, ascites and encephalopathy.

62
Q

What is the mechanism behind ascities?

A

Fluid in the peritoneal cavity
Inc pressure in the portal system causes fluid to leak out of capillaries.
Dec in circulating volume causes reduced BP in the kidents
This leads to increased aldosterone secretion via the RAAS.
Aldosterone leads to re-absorption of fluid and sodium retention -> increases hydrostatic pressure in the splanchnic vessels -> contributing to ascities
Cirrhosis causes a transudative (low protein) ascities.

63
Q

What are the different causes of ascities?

A

Cirrhosis
Heart Failure
Renal Failure/Nephrotic syndrome
Malignancy
TB
Pancreatitis

64
Q

What is the serum ascitic albumin gradient?
Why is it important to identify the cause of cirrhosis?

A

SAAG = (serum albumin) - (ascitis fluid album)
High (>1.1g/dL) : portal hypertension.
Lower that this is a non-portal hypertension cause.

65
Q

How common in spontaneous bacterial peritonitis?

A

Occurs in 10-20% of all patients with ascities
Mortality rate of 10-20%

66
Q

What is spontaneous bacterial peritonitis?
How does it present?

A

Infection in the ascitis fluid or peritoneal lining without a clear source.

Features: Fever, abdo pain, deranged bloods, ileus and hypotension

67
Q

What are the most common organisms causing spontaneous bacterial peritonitis?

A

Escherichia coli.
Klebsiella pneumoniae.

68
Q

What is the typical management of spontaneous bacterial peritonitis?

A

Ascitic tap
IV antibiotics as per local guidelines.

69
Q

What is the mechanism behind why portal hypertension is a problem?

A

The portal vein arises from superior mesenteric and splenic veins.
Liver cirrhosis increases the resistance to bloodflow in the liver.
This increases back-pressure throughout the portal system
This is called portal hypertension and can cause splenomegaly.
Collateral tortuous vessels at portosystemic anastomosis - distal oesophagus (varices) and anterior abdominal wall (caput medusa)

70
Q

What is the common management for hepatic encephalopathy?

A

Lactulose - laxative - reduce absoprtion time and makes acidic pH killing ammonia producing bacteria.
Antibiotics (rifaximin) - reduce amount of ammonia produced by GIT bacteria
Nutrition - prevent Wernicke (vitB1).

71
Q

What is the mechanism behind hepto-renal syndrome in liver cirrhosis?

A
  1. Portal hypertension causes portal vessels to release vasodilators
  2. Vasodilation of splanchnic vessels supplying GI organs
  3. Reduced blood pressure in the kidenys triggers the RAAS
  4. This leads to vasoconstriction of the renal vessels
  5. Renal vasoconstriction + decreases systemic pressure leads to hypoperfusion of the kidenys.
    This has a poor prognosis without a liver transplant.
72
Q

What are the different types of liver transplant?

A

Entire liver from deceased donor
Portion of liver from living donor (as liver regnerated)
Split donation - decreased donor liver split in two
All require life-long immunosuppression.

73
Q

What are the different scars seen in a liver transplantation?

A

Rooftop incision
Mercedes Benz 2 incision

74
Q

What are some factors suggesting unsuitability for liver transplantation?

A

Significant co-morbidities (severe kideny, lunf or heart disease)
Current illicit drug use
Continuing alcohol miuses (generally six months of abstinence is required)
Untreated HIV
Current or previous cancer (except certain liver cancers).

75
Q

What are the different classifications of liver cancer?
How is it tested for in liver cirrhosis?

A

Primary = commonly hepatocellular carcinoma
Secondary = mets from unknown primary source
Often presents late with a poor prognosis

Patients with liver cirrhosis are offered screening every 6 months: Ultrasound, Alpha-fetoprotein.

Med 2 (22 decks)

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