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YA - Interactive seminars/University lectures > GI - Chronic liver disease > Flashcards

GI - Chronic liver disease Flashcards

1
Q

(4) chronological types of chronic liver pathology

A
  • Advanced Liver Disease
  • Chronic Liver Disease (CLD)
  • Cirrhosis (clinical and histological meaning)
  • End-stage Liver Disease (ESLD)
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2
Q

List (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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3
Q

What are the (3) types of pictures of liver enzyme patterns?

A
  1. Hepatocellular injury or necrosis
    –Elevation of transaminases - ALT and AST
    –ALT predominantly from liver, AST from many sites
    –Very high ALTs in acute viral hepatitis, acute drug toxicity, ischaemia
  2. Intra or extra hepatic cholestasis
    –Elevation of alkaline phosphatase (also produced in other tissues esp bone)
    –Elevation of gamma glutamyl transpeptidase (GGT)
    –High ALP, GGT with minor elevation of transaminases typical of biliary obstruction, liver infiltration, cholestatic reactions to drugs
  3. Mixed picture
    –Seen in many forms of liver disease eg alcoholic liver disease, fatty liver disease
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4
Q

How do you diagnose CLD?

  • (4) symptoms
  • (3) clinical signs
  • (5) Ix
A

CLD may be suspected if risk factors present

•Symptoms:
–Fatigue, weight loss (muscle) or gain (ascites)
–Bleeding (haematemesis from varices)
–Abdominal distension (ascites)
–Confusion (encephalopathy)

•Clinical signs:
–Spider naevi
–Splenomegaly
–Jaundice

Ix:
•LFT’s (may be normal)
–Low albumin
–Raised bilirubin
–AST>ALT (AST not routine)

•Coagulopathy
–Prolonged INR (or high normal 1.2-1.3)
–Low platelets (or low normal, eg

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5
Q

What (3) do you look for on examination in chronic liver disease?

A
  1. Stigmata of chronic liver disease
  2. Signs of an underlying aetiology
  3. Signs of decompensation
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6
Q

What (7) are Stigmata of chronic liver disease?

A
  • Clubbing (arterial hypoxaemia)
  • Leuconychia (hypoalbuminaemia)
  • Palmar erhythema (excess oestrogen/altered microvasculature)
  • Dupuytren’s contracture (chronic liver disease due to alcohol)
  • Parotidmegaly (alcoholism)
  • Spider naevi (blanches on compression. Pathognomonic of cirrhosis if multiple)
  • Gynaecomastia
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7
Q

What (4) can cause Dupuytren’s contracture?

A
  • Chronic liver disease (alcohol)
  • Manual labour
  • Anti-epileptics
  • Diabetes
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8
Q

How many spider naevi is abnormal and what does it indicate?

A

> 2 abnormal

pathognomonic of cirrhosis if multiple

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9
Q

(2) causes of gynaecomastia

A
  • imbalance of estrogen:testosterone ratio

- secondary to medication e.g. spironolactone

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10
Q

Signs of DECOMPENSATION of chronic liver disease

A
  • Jaundice
  • Ascites/oedema
  • Coagulopathy (reduced clotting factors, thrombocytopenia)
  • Variceal bleeding
  • Hepatorenal syndrome
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11
Q

What could cause jaundice?

A
  • gallstones
  • HCC
  • portal vein thrombosis
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12
Q

Mechanism of ascites

A

Combination of reduced oncotic pressure (low albumin) + increased portal pressure

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13
Q

Ix of liver pathology

A
  • LFT
  • hepatitis A, B and C serology
  • ANCA (anti-neutrophil cytoplasmic antibody) for primary sclerosing cholangitis and autoimmune hepatitis
  • ANA
  • AMA (PBC), ASMA (anti-smooth muscle antibody), ALKM (anti-liver kidney microsomal antibody) for autoimmune hepatitis
  • Ultrasound
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14
Q

Briefly describe the histological progression from F0 to cirrhosis (F4)

A

F0 = normal
F 1 = peri-portal fibrosis, no septa

F 2 = peri-portal fibrosis with a few septa

F 3 = numerous septa, no architectural distortion

F 4 = architectural distortion & nodule formation

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15
Q

What are the big 3 causes of liver pathology?

A

–HBV
–HCV
–Alcohol

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16
Q

What are the (3) autoimmune liver pathology?

A

–Autoimmune hepatitis (AIH)
–Primary biliary cirrhosis (PBC)
–Primary sclerosing cholangitis (PSC)

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17
Q

What are the (3) metabolic liver pathology?

A

–Haemochromatosis (iron overload)
–Wilson’s disease (copper)
–Alpha 1-antitrypsin deficiency

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18
Q

What are the other (3) causes of liver pathology in the rule of 3’s?

A

–Fatty liver disease (NASH)
–Budd-Chiari (hepatic vein thrombosis)
–Chronic biliary obstruction
•eg tumour, cystic fibrosis

19
Q

What is hepatocellular carcinoma also known as?

A

Hepatoma (NOT benign)

20
Q

List (7) consequences of liver dysfunction

A
  1. Low levels of albumin/ clotting factors: coagulopathy, bleeding, ascites, oedema
  2. Failure to excrete bilirubin: jaundice
  3. Build up of waste products (ammonia): encephalopathy
  4. Portal Hypertension: ascites, splenomegaly, varices (+/- bleeding)
  5. Hepatorenal syndrome: essentially renal failure due to CLD
  6. Hepatocellular carcinoma (HCC): also in HBV in absence of cirrhosis
  7. Metabolic failure: hypoglycaemia (late), feminisation
21
Q

What does hepatic failure refer to?

A

presence of porto-systemic encephalopathy (PSE)

22
Q

In a chronic liver disease patient, what Ix should the pt have before a TOE procedure before a cardiac operation?

A

gastroscopy to screen for oesophageal varices

23
Q

(5) components in the Child-Pugh classification

A
  • encephalopathy
  • ascites
  • INR
  • Albumin
  • Bilirubin
24
Q

Mx of CLD with hepatic hydrothorax (ascites which tracks into pleural space)

A
  • Increased diuretics with spironolactone and frusemide
  • Occasional drainage via ultrasound
  • Replacement of fluid with IV concentrated albumin (NOT normal saline)
25
Q

Mx of CLD

  • treating the cause
  • Mx & prevention of Cx
A

•Treating the cause

•Managing and preventing complications
–Jaundice
–Bleeding varices
–Ascites (spontaneous bacterial peritonitis-SBP)
–Encephalopathy
–Hepatorenal syndrome
–Hepatocellular carcinoma
–Nutrition
–Osteoporosis
–Vaccination
26
Q

Mx of alcoholic hepatitis

A

Alcohol – abstinence
–? Inpatient detox/ withdrawal
–Support/ counselling
–Pharmacological (anti-craving medications)

27
Q

Mx of HBV hepatitis

A

– oral nucleos(t)ide analogues

– peg-interferon (IFN)

28
Q

Mx of HCV hepatitis

A

– peg-IFN + ribavirin +/- new agents

– not if decompensated CLD

29
Q

Mx of haemochromatosis

A

Venesection (drawing or removing blood from the circulatory system)

30
Q

Mx of autoimmune hepatitis (AIH)

A

Prednisolone +/- azathioprine/mercaptopurine

31
Q

Mx of Primary biliary cirrhosis (PBC)

A

Urso-deoxycholic acid

c.f. ERCP +/- stent or balloon dilatation occasionally in PSC

32
Q

Mx of Primary sclerosing cholangitis (PSC)

A

ERCP +/- stent or balloon dilatation occasionally

c.f. Urso-deoxycholic acid in PBC

33
Q

Mx of fluid retention in chronic liver disease

A

–Salt and fluid restriction
–Large volume paracentesis (ascitic tap)
–Diuretics (spironolactone/ amiloride, frusemide)

34
Q

Mx of bleeding varices

  • (3) sites
  • (2) Primary prophylaxis
  • secondary treatment
A

•Oesophageal, gastric, rare duodenal

•Primary prophylaxis
–Variceal band ligation (banding)
–Non-selective β-blockers (propranolol)

•Secondary treatment
–Octreotide or terlipressin
–Antibiotics (reduces bacterial translocation)
–Endoscopic banding (or sclerotherapy)
–Senstaken-Blakemore (SB) tube
–TIPSS (transjugular intrahepatic portosystemic stent/ shunt)

35
Q

(5) causes of encephlopathy in chronic liver disease

A 
•Drugs: Benzodiazepines, Alcohol, Narcotics
•Increased ammonia
–GI bleeding, constipation
–Infection
–Electrolyte imbalance, alkalosis, hypoxia
•Dehydration
•Portal vein thrombosis or primary HCC
•TIPSS
36
Q

What is a hepatorenal syndrome?

  • type I
  • type II
  • mechanism
  • Ix
A

–Worsening renal function in the setting of CLD

–Type I = acute (

37
Q

Why does cirrhosis increase risk of osteoporosis?

A

Vitamin D deficiency & physical inactivity

38
Q

Is liver transplant the cure for all CLD?

- how long will the graft survive

A

Transplant will cure many disorders but in HCV reinfection occurs 100% of the time

> 20yrs graft survival

39
Q

Indications for liver transplant

A

decompensated CLD

Recipients ranked according to MELD score

40
Q

Reasons for deferral of liver transplant

A

–Too early (liver function too good, MELD too low, eg MELD

41
Q 
What are (3) possible complications after liver transplant?
- How would you treat them
A
  • humoral rejection: plasmapharesis
  • CMV: ganciclovir
  • Anastomotic stricture: ERCP
42
Q

Who need screening for HepB?

A

Individuals from countries of high or intermediate prevalence (Aboriginals, Asia, Africa, South/central America, Caribbean etc)

  • Household contacts
  • Sexual contacts
  • IVDU, multiple sexual partners, MSM
  • Prisoners
  • Those with HCV, HIV
  • Dialysis
  • All pregnant women
  • All who receive immunosuppressive therapy
43
Q

How do you screen for HepB?

A
  • Hep B sAg
  • Hep B sAb
  • Hep B cAb
  • If Hep B sAg positive, refer to specialty clinic
  • If Hep B cAb positive, risk of reactivation with immunosuppression
44
Q

Briefly discuss the issue of hepatitis B in the community associated with liver cancer and how it can be resolved

A
  • There is a silent epidemic of liver cancer from HBV in Australia
  • Early detection of HBV and appropriate management significantly improves morbidity and mortality
  • A multimodal, culturally appropriate approach is required from communities, healthcare groups, government and politicians
  • Simultaneous interventions guided by research

YA - Interactive seminars/University lectures (87 decks)

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