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YEAR 3 - SEMESTER 2 > Case 8 - Alcoholic liver disease > Flashcards

Case 8 - Alcoholic liver disease Flashcards

1
Q

Compare the CAUSES of ACUTE and CHRONIC liver disease

A

ACUTE: toxins (e.g. paracetamol overdose) & hepatitis (A + E), malignancy, sepsis, severe hypotension

CHRONIC: alcohol, drugs (e.g. amiodarone), obesity, diabetes, HBV, HCV, cholestasis, autoimmune

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2
Q

Which types of hepatitis cause ACUTE vs. CHRONIC liver disease?

A

ACUTE: caused by hepatitis A & E

CHRONIC: caused by hepatitis B & C

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3
Q

What is the role of stellate cells in normal healing vs. chronic injury?

A

NORMAL HEALING: stellate cells transform into an ACTIVATED state and secrete ECM proteins (including collagen).

CHRONIC INJURY: the stellate cells remain activated for a prolonged period of time and secrete collagen to the point that the liver becomes FIBROTIC, causing a decline in hepatic function

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4
Q

What is the function of stellate cells in their quiescent form?

A

Vitamin A storage

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5
Q

What percentage of alcoholics develop cirrhosis?

A

~10 - 15%

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6
Q

Short-term ingestion of how many GRAMS of alcohol is enough to cause mild, reversible hepatic steatosis?

A

80 grams of alcohol over one - several days generally produces mild, reversible hepatic steatosis.

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7
Q

What is hepatic steatosis?

A

Accumulation of lipid droplets in hepatocytes which can turn into larger drops that distend hepatocytes.

Occurs after even mild alcohol consumption.

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8
Q

Is hepatic steatosis reversible?

A

YES - fatty change is completely reversible if there is abstention from further intake of alcohol.

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9
Q

How many grams of alcohol is in a standard drink?

A

10 grams

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10
Q

List the spectrum of alcoholic liver disease (from least to most severe - 4 stages)

A
  1. Hepatic steatosis (fat)
  2. Alcoholic Steatohepatitis (fat + inflammation)
  3. Cirrhosis (micro and macronodular)
  4. Hepatocellular carcinoma (HCC)
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11
Q

How does alcohol lead to steatosis?

A

Interferes with fat metabolism in the liver, increasing substrates for triglycerides

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12
Q

Each of the following are consequences of hepatic failure. List the clinical manifestations of each:

  1. Jaundice
  2. Impaired protein synthesis
  3. Encephalopathy
  4. Hyperdynamic circulation
  5. Hepatorenal syndrome
  6. Endocrine effects
  7. Skin changes
A
  1. Jaundice: yellowing of the skin and sclera
  2. Impaired protein synthesis: bleeding diathesis (lack of clotting factors), peripheral oedema (due to lack of albumin production), susceptibility to infections (complement)
  3. Encephalopathy: toxins normally filtered by the liver reach the BBB and adversely affect the waking centre of the brain (confusion, asterixis)
  4. Hyperdynamic circulation: lack of removal of toxins (e.g. NO) leads to hyperdynamic circulation –> bounding pulse
  5. Hepatorenal syndrome: liver failure leads to elevation of compounds (e.g. NO) that affect blood flow. Blood shunting from cortex to medulla, leading to renal failure.
  6. Endocrine effects: hyperaldosteronism, elevated oestrogen (e.g. testicular atrophy)
  7. Skin changes: spider navel
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13
Q

What sign can be found in hyperdynamic circulation?

A

Bounding pulse

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14
Q

Name 3 factors affecting an individual’s susceptibility to progress from hepatic steatosis –> steatohepatitis –> cirrhosis

A
  • Sex (females are more likely to get steatohepatitis)
  • Genetics
  • Alcohol metabolising gene polymorphisms
  • Diet & lifestyle (BMI, smoking)
  • Mitochondrial dysfunction
  • Co-existing conditions (e.g. chronic viral hepatitis, NAFLD)
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15
Q

Name 4 aetiologies of NON-ALCOHOLIC fatty liver disease (NAFLD) / non-alcoholic steatohepatitis

A

METABOLIC: T2DM, obesity
DRUGS: amiodarone
SURGICAL PROCEDURES: jejunoileal bypass

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16
Q

Gynaecomastia, spider navei, and palmar erythema can occur due to hepatic failure. What hormone is responsible for these signs?

A

Elevated OESTROGEN causes these signs

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17
Q

Compare the clinical features of COMPENSATED vs. DECOMPENSATED cirrhosis

A

COMPENSATED: asymptomatic or nonspecific symptoms (e.g. weakness, weight loss, fatigue)

DECOMPENSATED: asterixis, hepatic encephalopathy, easy bruising, jaundice, ascites, variceal bleeding

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18
Q

Excess accumulation of which molecule is seen in alcoholic liver disease?

A

NADH

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19
Q

Describe how the clinical features progress as alcoholic liver disease worsens

A
  1. ALCOHOLIC STEATOSIS: mostly asymptomatic, but patients can present with hepatomegaly and a sensation of pressure in the upper abdomen
  2. ALCOHOLIC STEATOHEPATISIS: nonspecific sx (nausea, abdo pain, weight loss, anorexia, low-grade fever w/tachycardia), possible jaundice
  3. ALCOHOL-RELATED CIRRHOSIS: nonspecific features PLUS:
    - Jaundice, pruritus
    - Spider navei, gynaecomastia, palmar erythema
    - Dupuytren’s contractures
    - Petechiae + purpura
    - Hepatosplenomegaly
    - Ascites
    - Asterixis
    - Fetor hepaticus
    - Peripheral oedema
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20
Q

What is the pathophysiology behind ascites in liver cirrhosis?

A
  1. Cirrhosis –> portal hypertension –> increased blood pressure in hepatic circulation –> increased hydrostatic pressure in abdominal capillaries –> fluid exudes from plasma into peritoneal cavity –> ascites
  2. Cirrhosis –> decreased albumin synthesis –> decreased plasma oncotic pressure –> fluid extravasates from intravascular space into peritoneal cavity –> ascites
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21
Q

How does chronic liver disease lead to excess oestrogen?

A

Decreased oestrogen clearance by the dysfunctional liver causes it to build up in the blood

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22
Q

Patients with ALD often have coexisting dysfunction in other organs. Name some of these.

A
  • Hepatorenal syndrome
  • Cardiomyopathy
  • Hepatic encephalopathy
  • Endocrine (inc. oestrogen)
  • Pancreatic dysfunction
  • Skeletal muscle wasting
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23
Q

What is the classic laboratory finding in ALD?

A

AST to ALT ratio >2

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24
Q

Accumulation of which compound is responsible for hepatic encephalopathy?

A

Ammonia

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25
Q

Which LFT abnormalities can be seen in ALD?

A
  • AST to ALT ratio >2
  • Raised GGT (common but nonspecific - typically much higher in chronic liver disease caused by alcohol)
  • Raised ALP
  • Raised bilirubin
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26
Q

Which markers of synthetic liver function will be abnormal in ALD?

A
  • Raised INR (dec. production of clotting factors)

- Low albumin

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27
Q

Abnormal CBE + iron studies in someone with ALD

A
  • Thrombocytopenia
  • Leukopenia
  • Macrocytic anaemia
  • Anicocytosis
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28
Q

What is a Rouleaux formation?

A

Stacking of RBCs that can be seen on a blood film.

Can cause raised ESR (which increases non-specifically with inflammation).

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29
Q

What is the imaging modality of choice in someone with suspected liver cirrhosis?

A

Liver ultrasound

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30
Q

What is the approach to management of liver disease?

A
  1. Treat the underlying cause
  2. Treat complications
  3. Avoidance of hepatotoxic substances (alcohol, NSAIDs)
  4. Routine vaccinations (pneumococcal, hepatitis, tetanus)
  5. Balanced diet, no protein restriction
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31
Q

Describe the role of the following pharmacotherapies in the treatment of liver disease:

  • Nonselective beta-blockers
  • Spironolactone, furosemide
A

BETA-BLOCKERS: lower portal pressure and prevent variceal bleeding

SPIRONOLACTONE, FUROSEMIDE: manage ascites & oedema in patients with hypoalbuminaemia

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32
Q

Name 3 surgical interventions for alcoholic liver disease

A
  1. PARACENTESIS: drainage of ascites to decompress the abdomen
  2. TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS): used to lower portal pressure and manage complications. Indicated for refractory ascites, recurrent oesophageal varices
  3. LIVER TRANSPLANT (only curative option for decompensated cirrhosis)
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33
Q

Which types of alcohol are worse for ALD?

A

Beer, spirits worse than wine

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34
Q

5-year survival data for COMPENSATED vs. DECOMPENSATED liver disease when patients ABSTAIN vs. CONTINUE DRINKING

A

COMPENSATED: 90% 5-year survival with abstention. 70% 5-year survival if drinking continues.

DECOMPENSATED: 60% 5-year survival with abstention. 30% 5-year survival if drinking continues.

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35
Q

Describe the clinical picture of someone with acute alcoholic hepatitis (history, PE, investigation)

A

History: heavy drinker

PE: tender hepatomegaly, jaundice, hepatic bruit, fever

Investigations: leukocytosis, elevated transaminases (AST>ALT 2), elevated GGT, elevated bilirubin, decreased albumin, elevated INR,

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36
Q

How many months of alcohol abstention is required for transplantation selection?

A

6 months

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37
Q

List the management for ALD

A
  1. Abstinence from alcohol / alcohol cessation
  2. Nutritional support (vitamin B12, zinc, thiamine, folate)
  3. Immunisations (hepatitis A and B - protect against further liver insults)
  4. Avoidance of hepatotoxins: medications, herbal supplements
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38
Q

How can someone be supported in their abstention from alcohol?

A
  • Counselling
  • Support groups
  • Pharmacological (disulfiram, acamprosate, naltrexone, Baclofen esp. if cirrhotic)
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39
Q

Name the pharmacological agents that can be used to help with alcohol abstention

A
  • Disulfiram (prevents usual metabolism of alcohol, creating unpleasant side effects)
  • Acamprosate
  • Naltrexone
  • Baclofen esp. if cirrhotic
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40
Q

Outline the nutritional supplementation required in ALD

A
  • High-energy nutritional supplementation
  • Thiamine (prevent Wernicke’s encephalopathy)
  • In alcoholic hepatitis: 4-7 small meals, with late evening food. Enteral supplements in patients with anorexia
41
Q

Decompensated alcoholic liver cirrhosis is defined when the patients has developed COMPLICATIONS. Name 4 of these complications

A
  • Ascites
  • Variceal bleeding
  • Encephalopathy
  • Hepatorenal syndrome
42
Q

Name 3 clinical manifestations of porto-systemic shunts

A
  • Oesophageal varices
  • Haemorrhoids
  • Caput medusa
43
Q

What is a porto-systemic shunt?

A

A port-systemic shunt occurs when venous blood accumulates in the portal system (e.g. due to liver cirrhosis, meaning that blood can’t pass from the hepatic portal vein –> IVC).

This blood backs up into SYSTEMIC veins and the increased pressure leads to varicose veins.

44
Q

What BP value defines portal hypertension?

A

> 12mmHg

45
Q

How does portal hypertension lead to hypersplenism (cytopenia due to enlarged spleen sequestering & destroying more blood cells)?

A

Portal hypertension –> blood backs up to the spleen –> splenomegaly –> overactive spleen –> increased destruction of blood products –> possible cytopenia (anaemia, leukopenia, thrombocytopenia)

46
Q

Name 5 consequences of portal hypertension

A
  • Hypersplenism / congestive splenomegaly
  • Oesophageal varices
  • Caput medusa
  • Haemorrhoids
  • UGIB due to portal hypertensive gastropathy
  • Hepatorenal syndrome
  • Ascites

https://www.youtube.com/watch?v=VTnAp-ngAXw

47
Q

ABCDE of portal hypertension

A 
A: ascites
B: bleeding
C: caput medusa 
D: diminished liver function
E: enlarged spleen
48
Q

What is the APRI?

A

AST to Platelet Ratio Index: determines the likelihood of hepatic fibrosis and cirrhosis in patients with hepatitis C.

<0.5 = free of fibrosis
>1.5 = cirrhotic
49
Q

What is the Child-Pugh score and how is it used?

A

5 components (ABCDE): albumin, bilirubin, coags (INR), distension (ascites), encephalopathy

Estimated liver cirrhosis severity.
CLASS A: 5-6 points = least severe liver disease. 5-year survival is 95%. Probably not cirrhotic?

CLASS B: 7-9 points = mildly severe liver disease. 5-year survival is 75%

CLASS C: 10-15 points = most severe liver disease. 5-year survival is 50%.

50
Q

What is the principle of ascites management?

A

To treat symptoms rather than completely remove the fluid. Symptomatic ascites requires management.

51
Q

How is ascites treated?

A
  • Sodium restriction
  • Adequate protein and energy intake
  • Diuretics
  • Large-volume paracentesis + IV albumin, TIPS, liver transplantation for severe refractory ascites
52
Q

Which diuretics are given for ascites?

A

Spironolactone or amiloride

+furosemide if the above are inadequate

53
Q

What is a red wale marking?

A

Endoscopic sign suggestive of recent haemorrhage or propensity to bleed. Seen in people with oesophageal varices.

54
Q

Outline the primary PREVENTION of bleeding gastro-oesophageal varices

A
  1. NONSELECTIVE BETA-BLOCKERS: carvedilol, propranolol

2. VARICEAL BAND LIGATION: banding of veins to cut off blood flow

55
Q

Outline the management of BLEEDING gastro-oesophageal varices

A
  1. EMERGENCY ENDOSCOPY w/ band ligation (banding)
  2. IV TERLIPRESSIN (vasoconstrictor) or IV OCTREOTIDE (growth hormone inhibition)
  3. Blood transfusion

if bleeding persists: balloon tamponade

56
Q

What is TIPS? What is it used for?

A

TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT

Connects the portal and hepatic veins, bypassing the liver. This reduces portal vein pressure and decreases the risk of variceal rupture + bleeding.

57
Q

What is the MOA, indication, and adverse effects of terlipressin?

A

MOA: vasoconstriction

INDICATION: bleeding oesophageal varices, hepatorenal syndrome

ADVERSE EFFECTS: abdominal cramps, headache, increased BP, pallor

58
Q

List 3 symptoms of uncomplicated and complicated alcohol withdrawal

A

UNCOMPLICATED: sweating, tachycardia, fever, tremor, poor concentration, anxiety, psychomotor agitation, disturbed sleep

COMPLICATED: dehydration + electrolyte imbalance, seizures, hallucinations or perceptual disturbances (visual, tactile, auditory), delirium

BOTH: anorexia, nausea, vomiting, dyspepsia

59
Q

Explain the CAGE questionnaire

A

C - have you felt the need to Cut down on your drinking?
A - have people Annoyed you by criticising your drinking?
G - have you ever felt Guilty about drinking?
E - have you ever felt you needed a drink first thing in the morning (Eye-opener) to steady your nerves or to get rid of a hangover?

60
Q

What is the AWS?

A

Alcohol withdrawal scale - rates perspiration, anxiety, tremor, agitation, temperature, orientation, etc.

https://adis.health.qld.gov.au/sites/default/files/resource/file/Withdrawal%20Scale%20-Alcohol.pdf

61
Q

What is SBP?

A

Spontaneous bacterial peritonitis

62
Q

How is SBP treated?

A

IV Ceftriaxone or cefotaxime

IV albumin for those with kidney impairment or jaundice (reduces risk of hepatorenal syndrome)

63
Q

Which 3 blood findings are useful for demarcating compensated vs. uncompensated liver disease?

A
  • Albumin
  • Bilirubin
  • INR
64
Q

Name 4 common causes of liver cirrhosis in developed countries

A
  • Chronic viral hepatitis (B, C)
  • Alcoholic liver disease
  • Haemochromatosis
  • Non-alcoholic fatty liver disease
65
Q

Painless jaundice is ______ until proven otherwise

A

Painless jaundice is CANCER until proven otherwise

66
Q

Name the 3 types of jaundice aetiologies and give 2 examples of each

A
  1. PREHEPATIC: haemolysis (over-production), impaired conjugation. (Gilbert’s)
  2. HEPATIC: viral hepatitis, HCC, metastases, alcohol, paracetamol, NAFLD
  3. POSTHEPATIC: intraductal (stones, cancer, strictures), extraductal (cancer, enlarged LN)
67
Q

Do LFTs tell you the fractions of conjugated and unconjugated bilirubin?

A

NO

68
Q

When are aminotransaminases released? What does the elevation indicate?

A

Aminotransaminases (e.g. ALT, AST) are released when there is breakdown of hepatocytes

Elevation indicates hepatocellular injury

69
Q

Aminotransaminase elevation >1000 indicates which cause of liver disease?

A

Viral hepatitis, drugs-induced injury, ischaemia

70
Q

Raised INR / PT indicates…?

A

Decreasing liver function

71
Q

If LFTs are normal other than isolated hyperbilirubinaemia, what test should be done next?

A

Fractionated bilirubin

72
Q

What is the pathophysiology behind hepatic encephalopathy?

A

Cirrhosis –> decrease in functioning hepatocytes –> gut-derived neurotoxins & ammonia not removed/metabolised/processed as effectively –> hepatic encephalopathy

73
Q

Describe the 4 stages of hepatic encephalopathy

A

Class I = apathy, insomnia, slowed intellect, restlessness
Class II = asterixis, lethargy, drowsiness
Class III = stupor but rousable, hyperreflexia
Class IV = coma, non-responsive to pain

74
Q

How is hepatic encephalopathy managed?

A
  • Low-protein diet

- Lactulose (laxative effect, lowers faecal pH to decrease ammonia absorption)

75
Q

How is hepatic encephalopathy managed?

A
  • Low-protein diet
  • Lactulose (inc. gut motility to dec. bacterial growth in gut)

(prevent further neurotoxins entering the blood)

76
Q

Which 2 mechanisms contribute to portal hypertension?

A
  1. Cirrhotic liver –> increased intra-hepatic resistance to flow
  2. Increased splanchnic blood flow due to excess release of endogenous vasodilators (e.g. NO)
77
Q

Increased portal pressure diverts blood flow to 5 systemic anastomoses. Name these

A
  1. Oesophagus: oesophageal varices
  2. Rectum: internal haemorrhoids
  3. Umbilicus: caput medusae
  4. Posterior abdominal wall
  5. Bare area of liver
78
Q

Describe the 3 pathophysiological mechanisms contributing to ascites

A
  1. Cirrhosis –> PORTAL HTN –> increased hydrostatic pressure
  2. Splanchnic/systemic vasodilation –> dec. renal flow –> increased RAAS –> fluid overload
  3. Decreased liver function –> less albumin –> less plasma ONCOTIC pressure
79
Q

How is ascites managed?

A
  1. Spironolactone

2. Paracentesis

80
Q

What is a side effect of spironolactone that can mimic liver disease signs?

A

Gynaecomastia

81
Q

Name 3 non-alcoholic causes of liver disease

A
  • NALFD
  • Viral hepatitis
  • Haemochromatosis
  • Alpha-1 antitrypsin deficiency
  • Wilson’s Disease
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Primary sclerosis cholangitis (highly associated w/UC)
82
Q

People who drink alcohol excessively can develop tolerance and dependence. Describe the underlying mechanism for this.

A

Alcohol consumption INCREASES the activity of GABA, an INHIBITORY neurotransmitter, on the GABA receptors. Over time, there is a down-regulation of GABA receptors.

As they gain this tolerance and dependence they start to feel very unwell when they don’t drink.

Stop drinking –> loss of inhibitory effect of GABA –> CNS overactivity, sympathetic overexcitement –> tachycardia, HTN, tremor, diaphoresis, etc.

83
Q

What is the first-line therapy for primary PREVENTION of variceal bleeding? Why?

A

Non-selective beta-blockers are first-line because they have additional benefits for prevention of other decompensatory events (e.g. ascites)

CARVEDILOL OR PROPRANOLOL

84
Q

How do nonselective beta blockers help prevent variceal bleeding?

A

Nonselective beta-blockers block Beta-2 receptor-mediated dilation in the mesenteric arterioles, resulting in vasoconstriction and decreased portal blood flow

Also decreases HR and thereby portal pressure. Carvedilol has additional vasodilator properties that decrease portal pressure even more

85
Q

List the stepwise progression of treatment for oesophageal varices (least to most severe)

A

Nonselective beta-blockers –> variceal band ligation –> terlipressin, variceal band ligation –> balloon tamponade –> TIPS

86
Q

Which patients qualify for variceal band ligation?

A
  • Imminent risk of variceal rupture
  • Beta-blockers contraindicated
  • Nonadherent to beta-blockers
  • HR not sufficiently lowered on nonselective beta-blockers
87
Q

Are prophylactic antibiotics given for bleeding gastro-oesophageal varices?

A

YES - ceftriaxone or ciprofloxacin

88
Q

What does the management of BLEEDING gastro-oesophageal varices involve?

A
  1. Endoscopic treatment
  2. Vasoactive agent (e.g. terlipressin)
  3. Prophylactic antibiotics
89
Q

Name 1 important complication of the TIPS procedure

A

Hepatic encephalopathy; since the creation of a shunt allows toxins (e.g. ammonia) to bypass the liver and enter directly into systemic circulation

90
Q

What are the Australian national guidelines for safe levels of alcohol consumption?

A

No more than 10 standards in a week. No more than 4 in one day.

91
Q

List the components of the porta hepatis from anterior to posterior

A

DAVE:

D - ducts (R & L hepatic duct)
A - arteries (R & L hepatic arteries)
V - vein (portal vein)
E - epiploic foramen (of Winslow)

92
Q

Describe the appearance of a cirrhotic liver

A
  • Fat accumulation in hepatocytes
  • Fibrous septa + regenerative nodules
  • Perivascular necrosis of central veins
93
Q

Which investigations would you order in someone with alcoholic liver disease / cirrhosis? Justify.

A
  1. CBE: elevated WCC, thrombocytopenia
  2. IRON STUDIES: macrocytic anaemia (B12, folate deficiency)
  3. COAGULATION STUDIES: low albumin, increased INR, clotting factor deficiency
  4. LFTs: raised bilirubin, AST:ALT >2, raised ALP, raised GGT (commonly raised in chronic liver disease due to alcohol)
  5. EUC: hyponatremia (ascites), high creatinine (hepatorenal syndrome)
  6. LIVER US: visualise liver cirrhosis
  7. SERUM ALPHA FETO-PROTEIN (AFP): if you suspect HCC
  8. VIRAL SEROLOGIES: hepatitis screen
94
Q

What is the pathophysiology underlying hepatorenal syndrome?

A

Cirrhosis/Portal hypertension –> accumulation of vasodilators (e.g. NO) –> splanchnic vasodilation –> decreased renal perfusion –> afferent arteriole vasoconstriction –> RAAS activation

  • Rise in serum creatinine
  • Low sodium excretion
  • Oliguria
95
Q

List 4 things that can exacerbate hepatic encephalopathy

A
  1. Renal failure
  2. Infection
  3. Constipation
  4. Upper GI bleed
  5. Diuretic therapy (can be due to electrolyte disturbance OR dehydration)
  6. Medications: drugs that act on the CNS (opiates, Benzos)

https://emedicine.medscape.com/article/186101-overview#a5

96
Q

Which electrolyte abnormalities are caused by spironolactone?

A
  • Hyperkalemia
  • Hyponatremia
  • Hypochloraemia (when combined with thiazides)
97
Q

Which electrolyte abnormalities are caused by furosemide?

A
  • Hypokalemia
  • Hyponatremia
  • Hypochloraemia
  • Hypocalcemia
98
Q

Which electrolyte abnormalities are caused by furosemide?

A
  • Hypokalemia
  • Hyponatremia
  • Hypochloraemia
  • Hypocalcemia

YEAR 3 - SEMESTER 2 (12 decks)

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