MET3 Revision: Hepatology I Flashcards

1
Q

A 55-year-old male alcoholic with known cirrhotic liver disease is admitted to the Gastroenterology Ward with a distended abdomen, jaundice and confusion. On examination, he is clinically jaundiced and has a massively distended abdomen with evidence of a fluid level on percussion. An aspirate of fluid is taken from his abdomen and sent for analysis. Results indicate the fluid is an exudate.

Which of the following is an exudative cause of ascites?

Portal hypertension

Cardiac failure

Fulminant hepatic failure

Budd–Chiari syndrome

Malignancy

A

A 55-year-old male alcoholic with known cirrhotic liver disease is admitted to the Gastroenterology Ward with a distended abdomen, jaundice and confusion. On examination, he is clinically jaundiced and has a massively distended abdomen with evidence of a fluid level on percussion. An aspirate of fluid is taken from his abdomen and sent for analysis. Results indicate the fluid is an exudate.

Which of the following is an exudative cause of ascites?

Malignancy

Ascites is defined as an accumulation of fluid within the peritoneal cavity. The causes can be classified according to the protein content of the fluid: < 30 g/l transudate, >30 g/l exudate. The most common causes of an exudative ascites are infection or malignancy. The above patient scenario would be more in keeping with a malignant cause.

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2
Q

Alcohol withdrawal sydrome serverity is determined using a scoring system from which chart? [1]

A

CIWA-Ar Chart

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3
Q

If a patient is scoring > [] on a CIWA-Ar then they are given a [] to help control symptoms

A

If a patient is scoring > 10 on a CIWA-Ar then they are given a benzodiazapene to help control symptoms

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4
Q

State the first and second line benzodiazepenes used to treat AWS [2]

A

1st line: Chlordiazepoxide

2nd line: Lorazepam - First line if cirrhotic.

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5
Q

Which drugs are used if seizures [1] and pyschotic symptoms [1] develop from AWS?

A

Seizures: IV Lorazepam

Pyschotic symptoms: Haloperidol (blocks D2 receptors)

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6
Q

Which drug is used to prevent Wernicke’s encephalopathy or Korsakoffs? [1]

What is given as continuing supplementation after ^? [1]

A

Prevent WE & Korsakoffs: Pabrinex: high strength Vit B & C

After completin pabrinex: Thiamine 100mg 3XD}

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7
Q

Why is Lorazepam prescribed for AWS in Ptx w cirrhosis? [2]

A

Short acting: liver function is already impaired, so if give long acting chlordiazepoxide then could get accumulation & cause toxicity (like resp. depression)

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8
Q

What is the treatment dose for pabrinex in treating AWS? [1]
What is the prophylatic dose for pabrinex in treating AWS? [1]

A

TD: 2 pairs IV pabrinex 3xday for 3-5 days
Prophylatic dose: 1 pair 3xD}

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9
Q

Name an AE of pabrinex [2]

A
  • Risk of anaphylaxis
  • Risk of glucose infusions in diabetic or low blood sugars: may deplete thiamine stores and precipate Wernickes
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10
Q

Describe and explain treatment plan for hepatic encephalopathy [3]

A

1. Lactulose:
- Increases faecal bulk & peristalsis
- Also reduces colonic pH: reduces absorption of NH3
- dose varies from 15-50ml TDS

2. Phosphate enemas:
- fast acting osmotic laxative
- STAT if Ptx encephalopathic; after passing stools PRN BD

3. Rifaximin
- antibiotic: diminishes deaminating enteric bacteria to decrease production of nitrogenous compounds
- 550mg BD

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11
Q

When is rifaximin prescribed in HE? [1]

A

Only in recurrent HE

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12
Q

Treatment of ascites? [2]

A

Fuoresemide:
- loop diuretic: binds to Na-K-2Cl; inhibits Na+ reabsorption
- 40mg OM
- IV in ascitic patients due to risk of AKI

Spironolactone:
- aldosterone antagonist at DCT
- 100mg OM; increased to 400mg if need

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13
Q

Which patients does terlipressin prescription need to be cautious with? [2]

A

Cardiac conditions:
Causes increase in BP; atherosclerosis; cardiac dysrythmia or coronary insufficiency

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14
Q

Tx for gastro-oesophageal varices? [2]

A

Terlipressin:
- contracts smooth oesophageal muscles; compression of the varices
- 1-2 mg for 4-6hrs until bleeding controlled
- Continue for 5day

Carvedilol:
- preffered due to mild anti-alpha 1 adrenergic activity (historically propanolol)
- used as prophylaxis

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15
Q

Tx for paracetamol OD? [1]
Describe MoA [1]

A

N-acytlcysteine (NAC) IV infusion:
- restores gluthathione levels or acts as alternate substrate for conjugation
- antioxidant
}}

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16
Q

Describe IV NAC infusion regime in paracetamol OD [3]

A

First infusion:
- 150mg/kg: one hour

Second infusion:
- 50mg/kg: 4 hours

Third infusion (can repeat if need)
- 100mg/kg: 16 hours

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17
Q

Tx for Hep B? [2]

A

Tenofocir
- competitive inhibition: replaces the deoxyribonucleitde substrate in HBV DNA
- faster acting than entecavir
- safe in pregancy

Entecavir
- inhibits RT of Hep B DNA
- toxicity in pregnancy

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18
Q

Describe the aim of Hep B treatment? [1]

Describe treatment aim of HCV? [1]

A

HBV: Suppress but DO NOT cure virus: undetectable viral load
HCV: CURE of virus

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19
Q

What monitoring should be given for HBV treatment? [1]

Why? [2]

A

Renal monitoring: nephrotoxicity due to lactic acidosis and may decrease bone mineral density

  • Monitor phosphate and creatinine levels
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20
Q

HCV treatment? [1]

A
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21
Q

Describe what is meant by Korsakoff syndrome [1]

A

Korsakoff syndrome is a chronic amnesia resulting from unrecognized or undertreated Wernicke encephalopathy and is caused by thiamine (vitamin B1) deficiency.

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22
Q

Name three scoring systems used to assess NAFLD [3]

NICErecommends considering the use of which test to assess the risk of advanced liver fibrosis in people with suspected non-alcoholic fatty liver disease (NAFLD), prior to the other two? [1]

A

NAFLD Fibrosis Score (NFS)
Enhanced Liver Fibrosis (EFS) - NICE rec. as first line score
FIB-4

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23
Q

Which pathology would these nails indicate? [1]

A

Wilsons disease

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24
Q

Why does Wilsons disease lead to haemolysis? [1]

A

The hemolysis in Wilson’s disease is due to deficiency of ceruloplasmin, the copper transport protein which results in exessive inorganic copper in the the blood circulation, much of it accumulates in red blood cells.

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25
Q

State two haemodynamic conseqeunces of:

  • Acute liver failure [2]
  • Chronic liver failure [5]
A

Acute liver failure:
* Cerebral oedema;
* Renal failure

Chronic liver failure:
Portal HTN:
* i) Ascites
* ii) Splenomegaly
* iii) Varices
* iv) Hepatic encephalopathy

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26
Q

Explain specific change in blood flow from portal hypertension contributes to hepatic encephalopathy [1]

A

Collaterals between splenic and renal veins: spleno-renal shunts: allow blood from bowel to bypass the liver and leak into systemic circulation, ammonia included (instead of being converted to urea and excreted). Goes to brain

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27
Q

What effect does portal HTN have on cell count? [1]
Why? [1]

A

Causes pancytopenia (red blood cells, white blood cells and platelets decreased) due to splenomegaly

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28
Q

How does portal hypertension lead to ascites? [5]

A
  • Increased pressure in portal system causes fluid to leak out of the capillaries in the liver and into peritoneal cavity. Increase in pressure also causes release of splachnic vasodilators.
  • Drop in circulating volume due to vasodilators on splachnic vessels and fluid forced out causes reduced pressure in kidneys
  • Renin is released
  • Aldosterone is secreted via RAAS
  • Increased aldosterone increase Na+ and therefore fluid reabsorption
  • Cirrhosis is causes low albumin levels, which decreases oncotic pressure
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29
Q

What are the two reasons that ammonia builds up in the blood in patients with cirrhosis? [2]

A
  1. liver cells’ functional impairment prevents them from metabolising the ammonia into harmless waste products
  2. collateral vessels between the portal and systemic circulation mean that the ammonia bypasses the liver and enters the systemic system directly
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30
Q

Which factors make hepatic encephalopathy worse? [5]

A

Constipation
Dehydration
Electrolyte disturbance
Infection
Gastrointestinal bleeding
High protein diet
Medications (particularly sedative medications)

31
Q

Describe the colour of urine & stools in ptx with CLD [2]

A

Light stool
Dark urine
Because bilirubin does NOT enter the bowel

32
Q

Describe the cholestatic symptoms of chronic liver disease [3]

A
  • Jaundice
  • Pruritus: due to buildup of bile salts in your blood.
  • Dark urine, pale stools
33
Q

State 5 triggers for decompensated cirrhosis

A
34
Q

Explain different signs that occur in compensated cirrhosis? [8]

A

Palmar erythema:
- caused by elevated oestrogen levels

Gynaecomastia and testicular atrophy:
- due to endocrine dysfunction

Jaundice:
- by raised bilirubin

Hepatomegaly (enlargement of the liver)

Bruising:
- due to abnormal clotting

Leukonychia (white fingernails)
- associated with hypoalbuminaemia

Ascites (fluid in the peritoneal cavity)

Excoriations (scratches on the skin due to itching)

Spider naevi (telangiectasia with a central arteriole and small vessels radiating away)

Clubbing & dupuytrens contracture

Xanthomas (raised, waxy-appearing, frequently yellowish-colored skin lesions)

35
Q

How do you diagnose ascites? [3]

A
  • Clinical exam:
    i) peripheral oedema
  • Ascitic tap: test WCC & cytology for spontaneous bacterial peritonitis or malignancy caused ascites
  • A high gradient (SAAG >11) indicates portal hypertension and suggests a nonperitoneal cause of ascites
  • Liver ultrasound: confirms flow in portal system (normally is anti-grade, but once scarred it reverses into retrograde flow)
36
Q

Treatment for ascites? [5]

A
  • Low Na diet
  • Spironolactone
  • Furosemide
  • Paracentesis (removal of ascitic fluid; replacement of albumin is required)
  • TIPSS
  • Liver transplant
37
Q

How is spontaneous bacterial peritonitis diagnosed? [2]

A

Ascitic tap:
- WCC > 250 mm3 (neutrophils 80%)
- Gram -ve often

38
Q

Tx of SBP? [2]

A

IV antibiotics: IV cefotaxime
Human albumin solution

39
Q

What is the difference between HRS type 1 and type 2? [2]

A

HRS type 1: rapid renal failure after acute trigger (SBP)

HRS type 2: progressive renal failure

40
Q

Tx for HRS? [3]

A
  • Terlipressin (alsos selective vasodilation of renal vessels)
  • Human albumin solution (HAS)
  • Liver transplantation
41
Q

Describe the different grades of hepatic encephalopathy? [4]

A

Grade I: inattention, confusion, altered sleep pattern

Grade II: lethargy, asterixis, slight personality disorder, slurred speech

Grade III: aggression, rigor, clonus, somnolent

Grade IV: coma

42
Q

State 5 triggers of hepatic encephalopathy [6]

A
  • Constipation
  • Sepsis
  • GI Bleeding
  • Drugs: opiods, benzodiazepines, diuretics
  • Dehydration
  • Portal vein thrombosis
43
Q

Which drug classes can induce H.E? [3]

A

opiods, benzodiazepines, diuretics

44
Q

Describe the treatment for hepatic encephalopathy [3]

A

Lactulose: laxative that reduces NH3 production in bowel

Phosphate enema (relieve constipation)

Rifaximin: modulates the gut flora resulting in decreased ammonia production

45
Q

State the cause of jaundice

A
46
Q
A
47
Q
A
48
Q

Why may patients with cirrhosis be prescribed vitamin K? [1]

A

Patients with cirrhosis may have vitamin K deficiency, due to the malabsorption due to cholestatic liver disease; restores blood clotting ability

49
Q

The [] blood test is the first-line investigation for assessing fibrosis in non-alcoholic fatty liver disease.

What is key about this? [1]

A

The enhanced liver fibrosis (ELF) blood test is the first-line investigation for assessing fibrosis in non-alcoholic fatty liver disease.

It is NOT used in patients with other causes of liver disease.

The enhanced liver fibrosis (ELF) test is a blood test that measures three molecules involved in liver matrix metabolism to give a score reflecting the severity of liver fibrosis.

50
Q

What ELF scores indicate advanced fibrosis? [1]

What ELF score indicates that is unlikely advanced fibrosis? [1]

A

10.51 or above – advanced fibrosis

Under 10.51 – unlikely advanced fibrosis (NICE recommend rechecking every 3 years in NAFLD)

51
Q

Upon ultrasound imaging of non-alcoholic fatty liver disease, how would fatty changes appear? [1]

A

increased echogenicity.

52
Q

When ALT>AST, what are two most likely causes? [2]

A

acute viral hepatitis or acute drug toxicity

53
Q

AST is found in the liver and which other tissue? [3]

A

Heart, muscle & kidney

54
Q

ALP is released from which tissues? [3]

A

Bile cannalicluar
Bone
Placenta

55
Q

Which liver enzyme is particularly raised in patients with alcohol excess? [1]

A

GGT

56
Q

Which immunoglobulins are specifically screened for in a liver screen? [3]
Which diseases do they indicate may be more likely?

A

IgA: ALD
IgM: Primary biliary cholangitis (PBC)
IgG: Autoimmune hepatitis

57
Q

Which auto-antibodies are specifically screened for in a liver screen for:

  • PBC [2]
  • AIH [3]
  • PSC [1]
A

PBC: -
- AMA (anti-mitochondiral antibody):
- AMA M2 antibody

AIH:
- ANA (Antinuclear antibody);
- SCM (smooth muscle antibody);
- SLA (soluble liver antigen)

PSC:
- ANCA (Antineutrophilic cytoplasmic antibody)

58
Q

Which metabolic markers in a viral screen indicate that a patient is suffering from:

  • NAFLD [2]
  • Haemochromatosis [2]
  • Wilson’s disease [1]
  • A1AT [1]
A

NAFLD (high association with metabolic syndrome)
* Elevated Lipids;
* Elevated fasting sugar

Haemochromatosis
* Raised ferritin
* HFE homozygous

Wilson’s disease
* Low caeruloplasmin

A1AT:
* Presence may increase chance of alcohol related injury if a carrier

59
Q

Describe the process of TIPS [2]

A
  • shunt inserted into portal vein & into hepatic circulation
  • reduces portal pressure
60
Q

When is TIPS indicated? [2]

A

Treat bleeding in varices due to portal HTN
Ascites refractory to medical therapy

61
Q

TIPS increases the risk of which pathology? [1]

A

Hepatic encephalopathy

62
Q

State causes of acute liver failure [4]

A
  • Drugs: paracetamol; alcohol
  • Infection: Hep A / B / E
  • Poor Nutrition
  • Pregnancy
63
Q

Describe the clinical features of someone suffering from acute liver failure [5]

A
  • Jaundice
  • coagulopathy: raised prothrombin time: INR >1.5
  • Hypoalbuminaemia
  • Hepatic encephalopathy
  • Renal failure is common (‘hepatorenal syndrome’)
64
Q

Define acute liver failure [1]

A

Acute liver failure (ALF) is a rapid decline in hepatic function characterised by jaundice, coagulopathy (INR >1.5), and hepatic encephalopathy in patients with no evidence of prior liver disease

65
Q

What specific investigations would reveal that Ptx is suffering from paracetamol OD? [4]

A
  • Raised AST or ALTs (5x above normal levels)
  • ALP (2x above normal)
  • Metabolic acidosis: due to raised lactate levels
66
Q

How do you manage Ptx with ALF? [6]

A
  • Monitor for encephalopathy and conscious state.
  • Administer N-acetylcysteine in all patients with acute liver failure, regardless of aetiology
  • Insert a urinary catheter and monitor urine output hourly
  • Blood glucose should be monitored by nursing staff every 2 hours for hypoglycaemia.
  • Baseline tests depend on the history ie paracetamol levels following an overdose
  • Arrange USS abdomen with Doppler of hepatic veins
67
Q

Name three non-paracetamol medications can cause ALF [3]

A

Non-paracetamol medications: Statins, Carbamazepine, Ecstasy

68
Q

What is Budd-chiari syndrome? [1]

A

Budd-Chiari syndrome is a vascular liver disorder due to obstruction of hepatic venous outflow:

Describes a condition characterised by occlusion or partial occlusion of any, or all, the three major hepatic veins. This may occur with or without occlusion of the IVC.

69
Q

How can ALF lead to death? [5]

A

Most cases of ALF are associated with a direct insult to the liver leading to massive hepatocyte necrosis

As the condition progresses it can lead to a hyperdynamic circulatory state with low systemic vascular resistance due to a profound inflammatory response

This causes poor peripheral perfusion and multi-organ failure

Patients also develop significant metabolic derangements (e.g. hypoglycaemia, electrolyte derangement) and are at increased risk of infection.

Marked cerebral oedema occurs, which is a major cause of morbidity and mortality in ALF.

70
Q

Define Gilbert’s syndrome [1]

A

Gilbert’s syndrome is an autosomal recessive condition associated with intermittent raised unconjugated bilirubinaemia, resulting from a defective glucuronyl transferase. This is the enzyme involved in conjugation of bilirubin, and so the ability of patients to conjugate bilirubin is significantly reduced.

71
Q

Gilbert’s syndrome is defined by which four characteristics? [4]

A

The condition is defined by the four following characteristics, necessary for diagnosis:

  • unconjugated hyperbilirubinaemia
  • normal liver function
  • no haemolysis
  • no evidence of liver disease
72
Q

Expalin why in Gilbert’s syndrome, there is absence of bilirubin in the urine?

A

In unaffected individuals following conjugation, conjugated bilirubin is released into the bile and is either excreted in the faeces as stercobilin or reabsorbed in the circulation and excreted by the kidneys in the urine in the form of urobilinogen

In Gilberts: there is a defective glucuronyl transferase. This is the enzyme involved in conjugation of bilirubin, and so the ability of patients to conjugate bilirubin is significantly reduced. Unconjugated bilirubin is non-water-soluble; therefore, it cannot be excreted in the urine.

73
Q

Describe the clinical presentation of Gilbert’s syndrome [2]

A

Asymptomatic between episodes
Jaundice triggered by stress / infection / dieting, fasting, an operation, dehydration, intermittent illnes

74
Q

Which age group and sex does Gilbert’s syndrome normally effect? [1]

What is the treatment? [1]

A

Usually presents during adolescent years

No treatment is required for Gilbert’s syndrome.