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Gastroenerology (Long) > Chronic Liver Disease > Flashcards

Chronic Liver Disease Flashcards

1
Q

What are the risk factors for Chronic Liver Disease you should ask for in pRicmcp? (6)

A

ETOH

Hep B/C (vertical, IVDU, transfusion, tatoos, MSM, +++sexual partners)

FH (Haemochromatosis/Wilson’s)

Diabetes (NASH)

Autoimmune diseases (PBC/PSC - UC)

Drugs (methyldopa, INH, nitrofurantoin)

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2
Q

3 drugs that can cause chronic hepatitis?

A

Methyldopa

Isoniazid

Nitrofurantoin

Others: PTU, MTX, Amiodarone

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3
Q

Chronic liver disease / Cirrhosis - PRICMCP

A

P: when? symptoms (incidental, jaundice, pruritis, lethargy, abdominal pain/hepatitis, complications - ascites/SBP, GI bleeding, encephalopathy)

R: ETOH, Hep B/C (vertical, IVDU, transfusion, tatoos, MSM, +++sexual partners), FH (Haemochromatosis/Wilson’s), Diabetes (NASH), Autoimmune diseases (PBC/PSC - UC), Drugs (methyldopa, INH, nitrofurantoin)

I: biopsy, fibroscan (vibration/flicks with a probe on your R flank?)

C: top-down → encephalopathy (ask about reversal of sleep cycle for brownie points + for discussion!), varices/GI bleed, ascites/SBP, splenomegaly/pancytopaenia

Complication of therapies (e.g. anti-viral)

M: General & Specific

Non-pharmacological: vaccines (Hep A/B), ETOH abstinence, salt restriction, FR, nutritional supplements (e.g. Hepatamine - branched-chain AAs for encephalopathy)

Pharm: diuretics, lactulose/rifaxamin, BB, prophylactic Abx for SBP

Interventional: surveillance for varices and HCC (USS+AFP), TIPPS, surgery for HCC

Specific disease treatment: e.g. anti-virals

C: how is patient coping? current status/FU? compliance to therapies & surveillance

P: understand the impact of CLD? insight into prognosis?

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4
Q

CLD - examination? (5)

A

Signs of CLD: jaundice, anaemia, flap, spider naevi, gyneocomastia

Signs for the Cause: parotid swelling (ETOH), KF rings (Wilson’s), Xanthelasma (PBC)

Signs of portal HTN: ascites, splenomegaly, dilated veins

Sign of HCC: Hepatic mass

Signs of RVF (e.g. TR): ddx of hepatosplenomegaly & ascites

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5
Q

How would you investigate (TEST) this patient with CLD?

A

Can be used in any patients with CLD with known aetiology. Always exclude alternative/secondary causes that could be optimised.

T: confirm a) deranged function (LFTs - look for AST/ALT >2 - alcohol), b) diagnosis (depending on the primary disease) - liver biopsy, Fibroscan, hepatitis serology…etc, and c) ascitic tap to look for SAAG ≥1g/L (portal HTN), cytology and cell counts (SBP).

E: exclude secondary causes/contributory factors (i.e. liver panel)

Collateral Hx for alcohol, Bloods: HBA1C (NASH), AFP (HCC), Hepatitis serology/VL (B/C), EBV, CMV, HIV, iron studies (haemoC), ceruloplasmin, copper, alpha-1-antitrypsin, AI-Abs: anti-mitochondrial (PBC), SMA, anti-LKM1 , anti-liver cytosol (AIH). p-ANCA (if colonic symptoms - UC, maker of PSC). Imagings: USS / CT - assess texture of the liver (fat infiltration, nodularity, exclude obstruction), doppler (Budd-Chiary), MRCP (PSC/PBC), Biopsy

S: assess for severity of disease - INR, Albumin, bilirubin, PLT (portal HTN), Na (hyponatraemia)

S: screen for the complication of disease - FBC (Anaemia, BM suppression), haematinics, EUC (hepato-renal), AFT/USS (Hepatoma) and Gastroscopy (varices)

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6
Q

What are the causes of ascites depending on the SAAG? (8, 4 each)

A

SAAG ≥ 11

  1. Portal HTN
  2. CCF
  3. Alcoholic hepatitis
  4. Budd-Chiari syndrome (hepatic vein thrombosis) or IVC obstruction

SAAG <11

  1. Peritoneal carcinomatosis
  2. Peritoneal TB
  3. Pancreatitis
  4. Nephrotic syndrome
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7
Q

What investigations would you organise for ascitic tap? (6)

A

SAAG - ?portal HTN, helpful for aetiology

Cell count and MCS - SBP, Ab sensitivity

Cytology - malignancy

Appearance - turbid or white

Lactate - raised in SBP

Amylase - pancreatic ascites

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8
Q

What are the causes of Budd-Chiary syndrome? (5)

A

Malignancy - solid or myeloproliferative (e.g. PRV)

OCP/Pregnancy (women)

PNH

Drugs (e.g. Azathioprine, Adriamycin)

Infection: schistosomiasis, amoebiasis

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9
Q

Budd-chiary syndrome investigation? (young people with abdo pain, hepatomegaly and ascites)

A

LFT - look for raised ALP

Ascitic tap - SAAG >11

USS + Doppler (85% sensitive)

MRA + MRV (diagnostic)

Liver biopsy (nutmeg liver)

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10
Q

Child-Pugh classification? (5). Max score? What are the moderate ranges (what are the numbers to remember)?

A

Essentially, each criterion denotes complications.

  1. Bilirubin (jaundice)
  2. INR (coagulopathy)
  3. Albumin (malnutrition)
  4. Ascites
  5. Encephalopathy

Scores up to 3 each categories, Max = 15.

Numbers to remember are 1.7-2.3 (INR), 30-35 (Albumin), 35-50 (Bilirubin) ⇒ anything within these ranges is “moderate” or 2-points.

Anything better = “mild” or 1-point

Anything worse = “severe” or 3-points.

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11
Q

Child-Pugh score - what are the scores for Grade A, B and C?

A

A: 5-6

B: 7-9

C: 10-15

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12
Q

What are the prognosis of this patient’s CLD? depending on Child-Pugh classification? (1-year and 2-year survival)

A

Roughly.

A: 100% (80%)

B: 80% (60%)

C: 40% (less than 40%)

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13
Q

Management of Ascites? (Goal/NP/P…etc)

A

Goal: 0.3 - 0.5kg weight loss/d (max 0.5kg/d) - i.e. gentle diuresis

Non-pharm

  • salt restriction (no added salt or salt-restricted diet based on dietician consultation)
  • fluid restriction (1.2L/d then titre according to FB)
  • nutrition (HPHE)

Pharm

  • Spinorolactone & furosemide (50:20mg ratio) and uptitrate every few days - monitor EUCs

Invasive

  • Paracentesis with albumin cover (max 10L drain) - regular program. Monitor INR/PLT (make sure INR <2.5 and PLT >50)
  • TIPPS: only if synthetic function ok, not coagulopathic, cardiac function OK (increases venous return ⇒ CCF), Exclude PVT
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14
Q

Why do you think TIPPS was not considered in this cardiac patient?

A

As TIPPS can cause increase in pre-load and overload RV

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15
Q

Management of Encephalopathy?

A

Goal: prevent deterioration, prevent recurrence

Non-pharmacological

  • nutrition and supplementation with branched-chain amino acids (hepatamine)
  • Consider impact on driving

Pharmacological:

  • Treat the cause: infection (most common), electrolyte disturbances (especially hypokalaemia), large protein meal, constipation.
  • Lactulose (BD dosing, titrate to achieve _2-3 bowel motions/_d), add rifaxamin (must be used in combination).
  • Avoid sedatives
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16
Q

What are the commonest causes / trigger of acute hepatic encephalopathy? (6)

A

Infection

HCC

Alcoholic binge

Electrolytes: especially, alkalosis (increases ammonia crossing BBB), hypokalaemia (increases renal ammonia production)

Constipation

High-protein diet

17
Q

Management of varices?

A

Acute

  • Resuscitation, transfuse if Hb <70, correct coagulopathy
  • Octreotide or terlipressin (1st line), ABx (reduces risk of re-bleeding), endoscopic variceal banding (or balloon tamponade)
  • If variceal banding (aka EVL - endoscopic variceal ligation) fails → reasonable to try endoscopic sclerotherapy. However if this fails,
  • TIPS - 90-100% success rate in reducing the bleeding (compared with surgery - high mortality rate)
  • Monitor for encephalopathy

Chronic

  • Non-pharm: Education re: portal HTN and potential complications. ETOH cessation
  • Pharm:
    • Primary prophylaxis: 10mg BD Propranolol → titrate to aim 55-60 HR or variceal banding (initial → repeat 6-8 weekly until eradicated → then annual scope)
    • Secondary prophylaxis: beta-blockade and banding program (also empirical ABx)
    • Consider TIPPS
18
Q

What are absolute contraindications for TIPPS (transjugular intrahepatic porto-systemic shunt)? (5)

A

Absolute contraindications are (basically infection or RF for RHF)

CCF

Severe TR

Severe pulmonary HTN

Active systemic infection

Biliary obstruction

Others (relative): encephalopathy, PVT

19
Q

HCC surveillance & Mx in brief…

A

6 monthly USS + AFP

If 3 x <3cm or 1 x <5cm → consider transplant. If not a candidate - RFA, resection

20
Q

What is the prognosis of patient who developed SBP?

A

1-yr survival is only 40%.

Consider referral to transplant centre

21
Q

When is primary prophylaxis for SBP recommended? (2)

A

Patients with cirrhosis and GI bleeding (shown to decreased mortality in RCTs)

Ascitic protein <15g/L and liver failure (CP ≥9, bilirubin >50)

22
Q

How is MELD score calculated (5 parameters)

A

MELD = model for end-stage Liver disease

INR

Bilirubin

Cr

Na

(note no albumin)

Hemodialysis (within last week - x 2)

23
Q

When should the patient be considered for liver transplantation (4)

A

MELD >15 (work-up patient from 10)

HCC (UCSF criteria - 1 x <5cm or 3 x <3cm in CP-B/C)

CLD with life-threatening complications - diuretics resistant ascites, recurrent variceal bleeding, encephalopathy or SBP, HPS, HRS

Acute liver disease (unlikely to result in spontaneous recovery)

However, consider early referal when 1) 1st episode of SBP or 2) progression to CP-B (7-8)

24
Q

What is your approach in managing this patient’s Chronic liver disease?

A

Goals

  • Identify & treat reversible/contributary/secondary causes
  • Slow progression of disease
  • Prevent complications

Confirm Dx

  • I would like to review LFT trends, synthetic functions, imagings, fibroscans, biopsies…etc

A - investigate for secondary causes/contributory factors

  • collateral Hx, HBA1C, Liver panel, Autoimmune panel, HIV, imagings
  • If Hep A/B Ab -ve vaccinate
  • Screen for depression

T: Non-pharm

  • Education: importance of adherence to therapies, complications, prognosis
  • Life-style: ETOH, smoking cessation, exercise, weight loss, marijuana - all can contribute to cirrhosis.
  • Nutrition: HEHP diet (at least 1g/kg/d + frequent meals), Hepatamine (branched-chain AAs), low salt (no salt in food, <2.5g/d), involve dietician
  • Infection: vaccinations - for Hep A/B if still no ABs, flu, hand & food hygiene
  • Cease hepatotoxic drugs - NSAIDs, paracetamol should be 2g max/d
  • OP: vitamin & calcium supplement, screen & treat OP

Pharm

  • Treatment of underlying cause
  • Lactulose + Rifaximine (HE)
  • Diuretics whilst carefully monitoring EUCs (ascites)
  • SBP prophylaxis (ABx) - secondary prophylaxis reduces recurrence & survival - otherwise 70% recur in 1 year
  • Propranolol 10mg BD (varices) + Variceal surveillance

Procedural***

  • Consider regular abdominal paracentesis with Albumin
  • Variceal surveillance: 6-8 weekly until eradication then annual
  • TIPPS
  • Discuss with transplant team when: 1) MELD 10-15, 2) CP-B (7-8), 3) 1st episode of SBP, 4) Hepatoma or 5) life-threatening complications

Involve family & GP for continued support and encouragement. Alcohol alliance.

Ensure F/U and screen & treat complications.

  • Clinical exam to detect new complications, monitor bloods.
  • 2-yearly DEXA
  • USS liver and AFP (HCC surveillance)
25
Q

Is there anything else (investigation wise) that could help you in deciding the dose titration of diuretics used for ascites (other than weight, renal function and Na)?

A

Urinary Na/K ratio (spot urine?)

If >1 (i.e. adequate excretion), aim spiro dose of 150mg/d

If <1 (i.e. low Na excretion) → increase the dose

26
Q

What is your approach to managing patient with persistent ascites despite high dose of diuretics?

A

Check adherence to fluid restriction and therapy. A helpful test is - urinary Na (24h).

  • If patient is truly diuretic resistant → Na excretion would be inadequate (<78mEq) → consider regular paracentesis / transplant
  • If Na excretion is adequate (>78mEq) → indicates non-compliance → educate
27
Q

What is your approach in managing suspected HRS?

A

Cease nephrotoxins

Identify & treat infection, especially SBP

Correct hypovolaemia (albumin)

Exclude alternative pathology before labeling patient as HRS - e.g. Hep B/C associated GN? - test for proteinuria and casts

Once there are no other cause and patient do not improve despite correcting above, diagnosis of HRS can be made - use vasoconstrictor and consider referral to transplant centre

28
Q

Useful investigatoins to distinguish between HRS vs. renal failure in liver patients of other causes? (3)

A

In True HRS

  1. Urinary sediment is benign
  2. No or minimal proteinuria
  3. Very low Na excretion (urine Na 10mEq/L)
29
Q

Where does varices develop in Cirrhosis?

A

Most commonly oesophagus, stomach and rectum*.

Theoretically, it can develop anywhere within the GIT.

30
Q

Management of varices other than oesophageal or stomach? e.g. Rectum.

A

Endoscopic therapy is attempted but often unsuccessful.

1st step is TIPS - if this fails, surgical Mx required.

Gastroenerology (Long) (8 decks)

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