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Yr3 Revision: Condensed Notes > Hepatology II > Flashcards

Hepatology II Flashcards

1
Q
A
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2
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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3
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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4
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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5
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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6
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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7
Q

When is rifaximin prescribed in HE? [1]

A

Only in recurrent HE

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8
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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9
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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10
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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11
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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12
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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13
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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14
Q

HCV treatment? [1]

A
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15
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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16
Q

Which pathology would these nails indicate? [1]

A

Wilsons disease

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17
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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18
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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19
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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20
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

21
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
22
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
23
Q

State 5 triggers for decompensated cirrhosis

A
24
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)
25
Q

How is spontaneous bacterial peritonitis diagnosed? [2]

A

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

26
Q

Tx of SBP? [2]

A

IV antibiotics: IV cefotaxime
Human albumin solution

27
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

28
Q

Tx for HRS? [3]

A
  • Terlipressin (alsos selective vasodilation of renal vessels)
  • Human albumin solution (HAS)
  • Liver transplantation
29
Q

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

A

opiods, benzodiazepines, diuretics

30
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

31
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.

32
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)

33
Q

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

A

increased echogenicity.

34
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

35
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)

36
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

37
Q

Describe the process of TIPS [2]

A
  • shunt inserted into portal vein & into hepatic circulation
  • reduces portal pressure
38
Q

When is TIPS indicated? [2]

A

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

39
Q

TIPS increases the risk of which pathology? [1]

A

Hepatic encephalopathy

40
Q

State causes of acute liver failure [4]

A
  • Drugs: paracetamol; alcohol
  • Infection: Hep A / B / E
  • Poor Nutrition
  • Pregnancy
41
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’)
42
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
43
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
44
Q

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

A

Non-paracetamol medications: Statins, Carbamazepine, Ecstasy

45
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.

46
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.

47
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
48
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.

Yr3 Revision: Condensed Notes (46 decks)

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