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YA - Interactive seminars/University lectures > GI - Liver failure > Flashcards

GI - Liver failure Flashcards

1
Q

(7) Key Functions of the Liver

A
  • Synthesis of clotting factors (except factor 8)
  • Glucose homeostasis-gluconeogenesis, glycogen storage
  • Albumin synthesis
  • Conjugation and clearance of bilirubin
  • NH3 metabolism- the urea cycle
  • Drug metabolism and clearance
  • Immune - dealing with gut derived bacteria and bacterial products
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2
Q

What (3) can you check for routine liver function tests?

A
  • bilirubin
  • albumin
  • clotting profile
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3
Q

Which clotting profile tells you more about liver disease?

A

INR affected more by liver disease than APTT

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4
Q

Why may cholestasis lead to higher INR?

A

Due to poor absorption of fat soluble vitamins including vitamin K -> vitamin K deficiency -> reduced factors 2, 7, 9, 10 -> higher INR

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5
Q 
45yo female, 7 wks post total abdominal hysterectomy
•Increasing abdominal pain over 2 days
•Vomiting
•No bowel actions
•Anorexia
•Weight loss (10kg over last 7 weeks)
taking Paracetamol PRN, Mylanta PRN

Soft non-tender, distended abdomen

AXR - incomplete mid to distal small bowel obstruction

Dx?

A

Recurrent subacute bowel obstruction secondary to adhesions from previous TAH

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6
Q

Initial Mx of bowel obstruction

A

–Nasogastric tube
–Intravenous therapy and electrolyte replacement
–NBM
–Analgesia (paracetamol 1g QID strict)

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7
Q

(4) common causes of acute liver injury

A
  • Drug poisoning: paracetamol
  • Acute viral hepatitis: hepatitis A, hepatitis B, hepatitis C. Less common EBV, others
  • Idiosyncratic acute drug reactions
  • Ischaemia: Circulatory shock, acute severe heart failure
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8
Q

Ix for acute liver injury

A
  • paracetamol in blood
  • HCV Ab
  • IgM anti-HAV, IgG anti-HAV
  • HBsAg, HBcAg, HBsAb
  • Liver ultrasound
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9
Q

What do HBsAg, HBcAg, HBsAb tell you?

A

HBsAg: RECENT infection or vaccination

HBcAg: previous/current INFECTION ONLY with HepB

HBsAb: previous/current infection OR vaccination

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10
Q

What (7) are the common causes of acute hepatitis ?

A

1) Acute viral hepatitis
2) Drug related
3) Ischaemic hepatitis
4) Autoimmune
5) Acute Budd Chiari
6) Wilson’s disease
7) idiopathic

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11
Q

When (3 criteria) do you transfer patient to a liver transplant unit due to acute liver injury?

A

–INR > 1.5 and rising (except POD)
–Any encephalopathy
–Poor prognosis

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12
Q

What may Ingestion of 10 or more standard paracetamol tablets result in?

A

fulminant hepatic failure resulting in death within 5-7 days if unchecked

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13
Q

Define acute liver failure

A
  • Rapid deterioration of liver function in previously normal liver
  • Trey and Davidson 1970 : “jaundice to encephalopathy within 1.5, any encephalopathy, duration of illness (jaundice) up to 26 weeks
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14
Q

Intervention for paracetamol acute liver failure

  • when is it effective
  • mechanism
A

NAC (N-acetylcysteine)

100% effective if given within 8 hours of ingestion, regardless of dose ingested

–Acts as glutathione donor
–Reduces production of toxic metabolite (NAPQI)

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15
Q

Intervention for hep B acute liver failure

A

Antivirals

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16
Q

Intervention for Wilson’s acute liver failure

A

Chelation/Exchange

17
Q

Intervention for Budd Chiari acute liver failure

A

TIPS (transjugular intrahepatic portosystemic shunts)

I.e. shunt connecting hepatic vein with portal vein to allow portosystemic communication

18
Q

What is Budd Chiari syndrome? What is the classical triad of symptoms

A

a condition caused by occlusion of the hepatic veins (e.g. clot) that drain the liver.

Classical triad Px:

  • abdominal pain
  • ascites
  • liver enlargement.
19
Q

Describe primary & secondary Budd-Chiari syndrome and their common causes

A

Primary Budd–Chiari syndrome (75%): thrombosis of the hepatic vein

Related with:

  1. Polycythemia vera
  2. Pregnancy
  3. Postpartum state
  4. OCP
  5. Paroxysmal nocturnal haemoglobinuria
  6. Hepatocellular carcinoma
  7. Lupus anticoagulants

Secondary Budd–Chiari syndrome (25%): compression of the hepatic vein by an outside structure (e.g. a tumor)

20
Q

Intervention for Autoimmune acute liver failure

A

Steroids

21
Q

(3) roles for liver biopsy in acute liver failure

A
  • Quantify extent of liver injury
  • Establish aetiology
  • Guide to treatment
22
Q

What criteria do you use to choose patients for liver transplantation?

A

King’s college criteria

For identifying patients with poor prognosis who need transplantation

23
Q

What is the toxic dose of paracetamol?

  • 24 hours
  • 48 hours
  • > 48 hours
A
  • 24 hours – 200mg/kg or 10g - whichever is less
  • 48 hours – 150 mg/kg or 6g per day – whichever is less
  • > 48 hours – 100 mg/kg or 4g per day – whichever is less
24
Q

(2) common clinical scenarios of paracetamol OD fulminant hepatic failure

A
  1. Prolonged courses in fasting individuals: therapeutic doses
  2. Supra-therapeutic doses in alcoholics & often in short courses
25
Q

How does paracetamol metabolism occur in the liver?

A

95% of paracetamol is bound by glucuronide & excreted in bile

5% are metabolised by P450 to NAPQI. Some of them are conjugated with glutathione & hence non toxic.

But when both glucuronide & glutathione are used up, the unconjugated NAPQI cause hepatotoxicity.

26
Q

General Mx for paracetamol OD acute liver injury

  • prevention of absorption
  • symptomatic care
  • risk assessment
  • specific care
A

•Prevention of absorption
–Activated charcoal within 60 minutes of ingestion

•Symptomatic care
–Anti-emetics

•Risk assessment
–Dose based / plasma paracetamol concentration

•Specific care
–N-acetylcysteine

27
Q

Describe the use of activated charcoal & its SE

A

Used to treat poisonings and overdoses following oral ingestion.

  • not effective for a number of poisonings including strong acids or alkali, cyanide, iron, lithium, arsenic, methanol, ethanol or ethylene glycol
  • over-the-counter drug to treat diarrhea, indigestion, and flatulence.

SE:

  • pulmonary aspiration which can sometimes be fatal if immediate medical treatment is not initiated.
  • contraindicated when the ingested substance is an acid, an alkali, or a petroleum product.
28
Q

Describe the Mx of paracetamol OD for:

- 8 hours

A

measure serum paracetamol level

1-8hours:
- measure serum paracetamol level -> plot serum paracetamol level on nomogram, if over nomogram treatment line -> NAC infusion

> 8 hours:
- commence NAC infusion -> measure serum paracetamol level & ALT. Plot serum paracetamol level on nomogram, if over nomogram treatment line, continue NAC infusion till normalised ALT.

29
Q

Causes of chronic liver disease (the rule of 3/s)

A
  • Most common: Alcohol, HBV, HCV
  • Genetic: Wilson’s disease, Haemochromatosis, A1AT deficiency
  • Auto-immune: Primary biliary cirrhosis, primary sclerosing cholangitis, Autoimmune hepatitis
  • Other: NASH, drugs, budd chiari syndrome
30
Q

(3) genetic causes of chronic liver disease

A
  • Wilson’s disease
  • Haemochromatosis
  • A1AT deficiency
31
Q

(3) autoimmune causes of chronic liver disease

A
  • Primary biliary cirrhosis
  • primary sclerosing cholangitis
  • Autoimmune hepatitis
32
Q

(3) most common causes of chronic liver disease

A

Alcohol, HBV, HCV

33
Q

Ix for chronic liver disease to define the aetiology

A
  • HCV Ab
  • HBsAg, HBcAb, HBsAb
  • Caeruloplasmin (low in Wilson’s disease)
  • A1AT
  • Fe studies (haemochromatosis)
  • ANA, SMA, AMA (autoimmune)
34
Q

(3) Cx of chronic liver failure & hence preventive Mx

A
  • Hepatoma (patient needs screening)
  • Variceal bleeding (patient needs screening)
  • Ascites (needs prophylacic antibiotics)

YA - Interactive seminars/University lectures (87 decks)

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