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CSIM2 > Liver 2.37-44 > Flashcards

Liver 2.37-44 Flashcards

1
Q

Arthralgia in liver disease?

A

Haemochromatosis, Hep B, AIH.

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2
Q

Extent of AST/ALT rise and significance?

A

1.5-3* ULN = ALD/NAFLD; >3* ULN in viral/drug-induced/AIH.

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3
Q

Serology in AIH?

A

Raised ANA, anti-SMA (smooth muscle antibody) and IgG. May have history of AI disease.

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4
Q

Serology and folate in ALD/NAFLD?

A

Raised IgA (with low folate in ALD)

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5
Q

Testing for active Hep C?

A

RNA PCR/Ag.

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6
Q

Anti-HCV?

A

Could be current or past infection; need PCR to see if viraemic. 25% will clear spontaneously.

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7
Q

AST/ALT in ALD?

A

>

  1. Caused by low ALT activity.
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8
Q

Drugs that can cause CLD?

A

Paracetamol mainly acute; chronic inc. methotrexate, nitrofurantoin, amiodarone so good DHx needed.

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9
Q

Signs of CLD?

A

Nail clubbing, palmar erythema, spider naevi, gynaecomastia, paucity of pubic/axillary hair, testicular atrophy, small/irregular liver, anaemia, caput medusae

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10
Q

Signs of decomp CLD?

A

Drowsiness/hyperventilation/asterixis/fs/foetur hepaticus (encehalopathy), jaundice, ascites, leukonychia, peripheral oedema, ecchymoses, respiratory alkalosis.

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11
Q

Anaemia in CLD?

A

Can be 2ndary to GI bleed (PT prolonged), hypersplenism caused by portal HTN (megaloblastic), alcohol (macrocytosis).

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12
Q

Most common haem. abnormality in CLD?

A

Thrombocytopenia (haemodilution, splenomegaly, reduced thrombopoiesis).

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13
Q

Bloods suggesting ethanol use?

A

Very high GGT (not a reliable measure), macrocytosis, hyperuricaemia, hypertriglyceridaemia.

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14
Q

Lipid abnormality in obstructive jaundice?

A

Marked hypercholesterolaemia!

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15
Q

Most specific marker for hepatocyte damage?

A

Probably ALT/PT. PT also affected by vit K deficiency, warfarin, malabsorption etc.

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16
Q

Why give ADH/terlopressin in GI bleed (caused by ruptured varices)?

A

ADH stimulates vWF (terlopressin is ADH analogue); also reduces portal HTN.

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17
Q

Causes of ascites with low SAAG?

A

Peritoneal carcinomatosis, nephrotic syndrome, pancreatitis, serositis.

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18
Q

Acute vs chronic GI bleed MCV?

A

Acute is normocytic; may not be apparent until resuscitate. Chronic causes IDA so is microcytic.

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19
Q

Glasgow-Blatchford score?

A

Predicts likelihood of needing intervention following acute UGI bleed.

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20
Q

How to confirm Gilbert’s?

A

Suspect with isolated raised bilirubin; subsequent fasting bilirubin should be further elevated still.

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21
Q

Indications of advanced ALD?

A

Splenomegaly, other signs of portal HTN on USS, low platelets, low albumin, raised bilirubin.

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22
Q

PBC clinical features?

A

Raised ALP, +ve AMA (anti-mitochondrial antibodies), IgM elevated, F (:M 10:1), middle aged. ITCH, fatigue, poor cognition, (dry eyes/mouth [other AI disease]). May present with jaundice/advanced liver disease. See xanthelasma/xanthomas. Diagnosis: compatible history, cholestatic LFTs, +ve AMA (no biopsy needed). 2 = probable, 3 = definite. Biopsy can be helpful to stage.Granulomatous inflammation and obliteration of intrahepatic ducts. Bilirubin predicts prognosis.

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23
Q

Diseases associated with PBC?

A

RA, Sjogren’s (80% of cases).

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24
Q

Extrahepatic Cx of PBC?

A

Osteoporosis/osteopenia.

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25
Q

T1 AIH CFs?

A

ANA and anti-SMA +ve, IgG elevated. Any age. F:M 3:1. Hepatitic LFTs.

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26
Q

Diseases assoc. with AIH?

A

Coeliac, vasculitis, AI thyroiditis.

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27
Q

Diagnosing AIH?

A

Hepatic LFTs, autoantibodies, IgG elevated; usually need biopsy to stage/diagnose.

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28
Q

PSC CFs?

A

Hx of IBD (80%) (particularly UC). ALP elevated! p-ANCA +ve. M:F 2:1.

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29
Q

PSC presentation?

A
  1. Asymptomatic (raised ALP)
  2. Symptoms (itch much milder than PBC, fatigue, RUQ pain, weight loss, jaundice). Hepatomegaly (portal HTN due to sclerosis)
  3. Acute cholangitis.
  4. Malabsorption (due to inadequate bile release; low fat-soluble vitamins). Get steatorrhoea.
  5. Cirrhosis/Cx
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30
Q

Diagnosing PSC?

A

Cholestatic picture (+ ANCA). US/CT not helpful; MRCP shows ‘beads on a string’ with intra/extrahepatic dilatation and multiple strictures. 2/3 of cholestatic LFTs (high ALP), MRCP showing signs, +/- biopsy. If MRCP not diagnostic, ERCP can be done; if both normal then do liver biopsy (may show small duct PSC i.e same disease with normal MRCP findings). See ‘onion skin fibrosis’.

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31
Q

What must be screened for in PSC?

A

Cholangiocarcinoma (probably with USS/symptom surveillance), CRC (IBD).

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32
Q

Diagnosing/imaging in HCC?

A

Dynamic contrast MRI more sensitive and specific. 4 phase CT shows characteristic hypervascular (rich vasculature) lesion in arterial phase with washout (shunting) in portal venous/delayed phase. If not enough classical features present, do biopsy (but can diagnose from imaging alone).

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33
Q

AFP in HCC?

A

Elevated in 50-75% cases; in screening, has high specificity at levels over 200.

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34
Q

Assessing fitness for treatment in HCC?

A

Do performance status and Child-Pugh. If single nodule can resect; if have single nodule and portal HTN then cannot resect (transplant if no associated disease; RFA/PEI if do). If more advanced, do TACE to infarct tumour, or sorafenib, or palliate.

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35
Q

Eligibility for transplant in HCC (Milan criteria)?

A

Single tumour <5cm, or up to 3 <3, with no extrahepatic involvement or major vessel involvement. Larger tumours are likely to have locally spread so transplant useless.

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36
Q

Preferred treatment in early/optimal HCC?

A

Resection; impossible if have portal HTN etc. because need all of liver function possible!

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37
Q

Prognosis in HCC if resectable?

A

5YS = ~50%. If not the n~24 months median. Vast majority of HCC patients have cirrhosis so already have very bad survival.

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38
Q

How is NASH confirmed?

A

Biopsy

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39
Q

What is ‘advanced’ NAFLD based on?

A

Bloods, score, clinical picture. May be transplant candidate.

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40
Q

Courvoisier’s law?

A

In painless jaundice with enlarged (non-tender) gall bladder, cause is unlikely to be gallstones. Pancreatic or cholangiocarcinoma more likely. Gallbladder with stones is usually chronically fibrosed so cannot enlarge; get pain with acute obstruction ie stones not slow-growing cancer.

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41
Q

What is acute/fulminant hepatic failure?

A

Devastating clinical syndrome associated with rapid liver dysfunction, coagulopathy, encephalopathy (IN ABSENCE OF EXISTING LIVER DISEASE, IN LESS THAN 6 MONTHS)

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42
Q

Key markers for fulminant hepatic failure?

A

PT prolonged by 4-6 seconds, INR >1.5

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43
Q

Categories of acute liver failure?

A

Hyperacute = 0-7 days; acute = 8-28; subacute = 1-3 months.

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44
Q

Features of different classifications of ALF?

A

Cerebral oedema and raised PT more prominent (hyper)acutely; bilirubin least raised hyperacutely; prognosis best hyperacutely.

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45
Q

Causes of ALF?

A

Paracetamol (39%), idiosyncratic drug reaction, Hep A/B, indeterminate (17%).

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46
Q

NANB hepatitis?

A

Non Hep A/B.

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47
Q

What is seronegative hepatitis?

A

Idiopathic cause of acute liver failure; not Hep A-E. Does not include paracetamol OD etc.

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48
Q

Major and minor routes of paracetamol metabolism?

A

Major (saturable) route is to sulphate/glucoronide conjugates; minor route is to NAPQI, causing cell death (detoxified by glutathione to mercapturic acid conjugates).

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49
Q

What detoxifies NAPQI?

A

Glutathione

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50
Q

What is the role of NAC in paracetamol (acetaminophen) OD?

A

Replaces glutathione to allow detoxififcation

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51
Q

Which patients are high risk in paracetamol OD?

A

Malnourished, enzyme induction (alcohol, AEDs, rifampicin)

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52
Q

Key investigations in ?paracetamol OD?

A

INR, creatinine, glucose, ABG WITH LACTATE ammonia.

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53
Q

Why do Doppler US in ALF?

A

Can find ischaemia/thrombosis (inc. Budd-Chiari) to explain ALF.

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54
Q

Value of MRI liver size in ALF?

A

Good prognostic marker (unlikely to survive if under 750mls)

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55
Q

Why might ALT normalise in ALF?

A

Massive necrosis (bilirubin and PT likely to still be rising).

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56
Q

Differential of massive transaminitis/ALF?

A
  1. Vascular (hypotension, congestion, HAT)
  2. Viral
  3. Drugs/toxins (paracetamol, NSAIDs, statins, Abx [nitrofurantoin])
  4. Others (Wilson’s, AIH).
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57
Q

Three IC Cx of ALF?

A

HE, cerebral oedema, IC HTN.

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58
Q

Four changes to metabolic function in ALF?

A

Decreased:

  1. Gluconeogenesis (hypoglycaemia)
  2. Lactate clearance (lactic acidosis)
  3. Ammonia clearance (HE/hyperammonaemia)
  4. Synthetic capacity (coagulopathy).
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59
Q

Why get HE in ALF?

A

Liver unable to synthesise urea; brain detoxifies NH3 instead; produces glutamine; osmotic effect draws water in.

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60
Q

Grading HE?

A

1-4; 4 = GCS<8 ie coma.

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61
Q

Which two causes of ALF arguably have the poorest prognosis?

A

Wilsons, Budd-Chiari.

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62
Q

Key predictor for prognosis in paracetamol induced ALF?

A

Arterial lactate (strongly correlates with paracetamol levels)

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63
Q

Lipid abnormality in metabolic syndrome?

A

Raised triglycerides (not cholesterol)

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64
Q

Osteoporosis and obesity?

A

Not linked (low BMI more associated)

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65
Q

Features of NAFLD?

A

Simple steatosis, malignancy, liver cirrhosis, advanced fibrosis (not bile duct obstruction)

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66
Q

Examples of things that might make you ineligible for liver transplant?

A

Varices (suggests severe portal HTN and therefore will not tolerate), large HCC lesion or multiple lesions. Indications include resistant ascites and (repeated) HE.

67
Q

Diagnosing HEV?

A

IgM and IgG; + HEV RNA [gold standard] (stools/serum/liver biopsy)

68
Q

Problems with HEV IgM?

A

May get cross reactivity to EBV/CMV. Unreliable if immunosuppressed.

69
Q

Which patients are more at risk of fulminant liver disease with HEV?

A

Existing LD, IC, pregnancy! NB: HAV is very mild in children, HEV very bad in pregnancy.

70
Q

What Ix is diagnostic for cholangitis?

A

MRCP. Subsequent ERCP may be needed therapeutically.

71
Q

Liver mets/primary on US?

A

Classically hypoechogenic.

72
Q

Acute liver failure pathophysiology?

A

Massive hepatocellular necrosis; mainly in zone 3 ie centrilobular (around hepatic vein) which is the most hypoxic and therefore susceptible to injury.

73
Q

Cirrhosis pathophysiology?

A

Diffuse process where normal lobules are replaced by architecturally abnormal nodules separated by fibrous tissue. Decompensated cirrhosis = clinically evident complications (compensated may have no/few symptoms)

74
Q

Four/five principle manifestations of decomp. cirrhosis?

A

Ascites,GI bleed (ruptured varices), HE, jaundice, (+/- coagulopathy), hepatorenal syndrome

75
Q

Vascular changes in compensated cirrhosis?

A

Increased intrahepatic resistance -> moderate portal HTN; get splanchnic arterial vasodilation causing low effective circulating volume so CO and plasma volume are increased to compensate.

76
Q

Three sites of porto-systemic anastomosis?

A

“Butt, gut and caput”

  1. Rectum; get haemorrhoids
  2. Oesophagus (varices).
  3. Umbilicus (caput medusae).
77
Q

Vascular changes in decompensated cirrhosis?

A

SEVERE portal HTN (as disease progresses) leads to severe splanchnic vasodilation and markedly reduced EABV; get RAAS/vasopressin action causing ascites; further RAAS mediated vasoconstriction causes reduced CO and renal failure (hepatorenal syndrome). Also get translocation of bacteria in advanced disease leading to SBP.

78
Q

Key precipitant of hepatorenal syndrome?

A

SBP (particularly in ALD).

79
Q

Pathophysiology of hepatorenal syndrome?

A

“Underfill” caused by blood pooling in dilated splanchnic vessels leads to underperfusion and renal failure; RAAS activation only further constricts renal arterioles and exacerbates. Therefore occurs on a background of ascites (need advanced portal HTN) and often hyponatraemia.

80
Q

Precipitants of decompensated liver disease?

A

Infection (SBP/hepatitis/sepsis), drugs (NSAIDs, diuretics, opiates), surgery [anaesthesia], hypotension, alcohol increase, GI bleed, portal vein thrombosis, dehydration, HCC, constipation.

81
Q

Why can constipation cause decompensated liver disease?

A

Less able to remove toxins from stool; longer transit time = more toxins and liver is overwhelmed.

82
Q

Drivers of ascites?

A

Major is portal HTN (and RAAS); hypoalbuminaemia is relatively minor. Interventions are aimed at drainage/sodium restriction etc.

83
Q

What is SBP?

A

Infection of ascitic fluid in absence of 2ndary cause. Usually asymptomatic. Bacterial translocation in cirrhosis is main cause. Occurs in 10% hospitalised cirrhotics.

84
Q

Diagnosing SBP?

A

PMN>250 on ascitic fluid analysis.

85
Q

Ascites/hepatorenal syndrome spectrum?

A
  1. Subtle Na retention = preascites.
  2. Obvious Na retention = responsive ascites.
  3. Avid retention = refractory ascites
  4. Functional renal failure = hepatorenal syndrome.
86
Q

Two types of hepatorenal syndrome?

A
  1. Acute = 2ndary to a precipitant (SBP, paracentesis, sepsis, GI bleed). High mortality.
  2. Spontaneous, chronic. Usually in resistant/intractable ascites. Usually have hyponatraemia.
87
Q

Drugs to combat splanchnic vasodilation in preventing HRS?

A

Terlopressin, IV albumin.

88
Q

How do varices form?

A

High portal pressure forces blood to “shunt” through anastomosis to venous system instead; fragile, dilated veins appear.

89
Q

TIPSS procedure?

A

Shunt insertion to reduce portal HTN/variceal bleeds. Allows portal vein to bypass liver and enter hepatic vein. Used for refractory ascites, and rescue therapy in variceal bleed.

90
Q

Medical management for ascites?

A

Na + restriction and diuretics. Paracentesis allows symptomatic relief.

91
Q

Treatments for variceal bleed?

A

Terlopression (ADH analogue), antibiotics, banding/tamponade/sclerotherapy, TIPSS.

92
Q

Risk with TIPSS?

A

Get liver failure as reduce blood supply, and HE (reduced detoxification).

93
Q

What is HE?

A

Spectrum of neuro/psych problems seen in liver faulure; porto-systemic shunting and impaired function mean more toxins in blood.

94
Q

Ammonia in HE?

A

Elevated in 90% of HE, but useless as a diagnostic test

95
Q

Encephalopathy in CLD vs ALF?

A

Cerebral oedema far more common in acute.

96
Q

Main causes of HE?

A

Infection, GI bleed, electrolyte disturbance, CONSTIPATION, sedatives.

97
Q

Alcholic hepatitis and liver pathology?

A

Can cause chronic liver disease, acute on chronic or acute death.

98
Q

Key predictors for ALD response?

A

Dose-relationship, genetic variation, and, most importantly, obesity (synergy).

99
Q

Which feature of CLD is particularly prominent in PBC?

A

Xanthelasma/other xanthomas.

100
Q

Acute and chronic hepatitis?

A

Acute < 6 months; usually < 3.

101
Q

Which two hepatitides are RNA viruses?

A

C and E.

102
Q

Two investigations indicating Wilson’s?

A

Decreased serum caeruloplasmin and increased urinary copper.

103
Q

Extrahepatic manifestations of HEV?

A
  1. Neuro (expect HEV in CSF) inc. neuropathy [brachial neuritis w/ winged scapula]encephalitis, demyelination, GBS
  2. Renal (glomerulonephritis)
  3. Rheum (cryoglobulinaemia, arthralgia, myalgia)
104
Q

Persistent HEV in transplant recipients?

A

Defined when HEV RNA detectable in blood/stool for >3 months. Only causes modest transaminitis but can rapidly progress to cirrhosis so must test for RNA in IC patients with odd LFTs (and give dietary advice)

105
Q

Hep B?

A

Blood-borne, DNA, high incidence of vertical transmission (developing). Developed = sex/IVDU

106
Q

Hep B vertical transmission?

A

90% of babies infected vertically or perinatally develop chronic HBV. Vaccinations and HBIG can reduce this significantly.

107
Q

Natural course of HBV (if aquired in utero, say)?

A
  1. Immune tolerance.
  2. Immune clearance. [TREAT]
  3. Inactive carrier.
  4. Reactivation. [TREAT].
108
Q

Immune tolerance phase of HBV?

A

High HBV DNA and HBeAg; ALT low then rises. No Anti-Hbe. Asymptomatic. Childhood.

109
Q

Immune clearance phase of HBV?

A

(18-25) Transaminitis as attempt to clear; can get severe damage so treat! HBV DNA reduces, ALT up, HBeAg positive; becomes replaced by anti-HBe.

110
Q

Inactive carrier phase of HBV?

A

Low ALT, and HBV DNA. Anti-HBe present, HBeAg absent. Asymptomatic. ~50.

111
Q

Reactivation phase of HBV?

A

40-50. Immune system loses control, HBV DNA may rise (replication), ALT may raise. Need to treat.

112
Q

“Paths” in chronic HBV?

A

In immune clearance/reactivation, can go to cirrhosis (then decomp/HCC). Immunotolerant can go straight to inactive; inactive can go to sAg loss ie cleared.

113
Q

Key difference between immune clearance and reactivation?

A

Immune clearance is eAg+ve; reactivation is eAg-ve.

114
Q

HBsAg +ve?

A

Active HBV infection

115
Q

HBV DNA levels?

A

Levels of virus in blood

116
Q

HBeAg +ve?

A

High level of HBV replication therefore usually with HBV DNA; more infectious.

117
Q

Anti-HBcIgM?

A

Acute HBV

118
Q

Anti-HBcIgG?

A

Past or current HBV; differentiate with HBsAg.

119
Q

Anti-HBsAb?

A

Vaccination or past infection

120
Q

Anti-HBeAb?

A

Present in Inactive/Reactivation

121
Q

Monitoring in chronic HCC?

A

Cx of cirrhosis e.g varices, and HCC (6 monthly US, AFP).

122
Q

Aims for treatment in chronic HBV?

A

HBsAg->HBsAb = cure. Also, HBeAg->Ab, undetectable HBV DNA, reduced HBsAg, normalised ALT, improved histology.

123
Q

Hep C?

A

50-80% develop chronic carriage (therefore cirrhosis/HCC). Different genotypes with different treatment responses. UK transmission is 90% IVDU. Worth screening extensively as treatment is good.

124
Q

Natural history of Hep C?

A

Initial acute phase; after 6 months 20% clear it, 80% chronic carriage. Of those, 80% have slow/no progression to fibrosis; 20% get cirrhosis. Then high risk of LF/decomp/HCC/death (or transplant).

125
Q

What variable increases risk of cirrhosis in HCV?

A

Alcohol consumption! (among many others) As it is also profibrogenic and hepatotoxic.

126
Q

Fibrosis cellular?

A

Increased secretion and decreased degradation of ECM. ECM becomes more dense (mainly collagen). Activation of hepatic stellate cells and other myofibroblasts; sinusoidal cells lose fenestrations. This + accumulates ECM in SoD leads to reduced exchange -> hypoxia and dysfunction.

127
Q

How does fibrosis lead to portal HTN?

A

Hypoxia; liver responds with angiogenesis and increased HSC contractility; get increased sinusoidal resistance and generates portal HTN. Progressive fibrosis distorts normal acinar architecture.

128
Q

Main fibrogenic cell type?

A

HSCs (become myofibroblasts; essentially on spectrum before SM cells). Rapidly proliferating and migrate to site of injury.

129
Q

Causes of jaundice?

A

Alcoholic hepatitis, decompensated CLD, biliary obstruction (choledocholithiasis/malignancy), drug-induced liver disease; chronic mild jaundice in Gilbert’s, compensated CLD and haemolysis.

130
Q

Fine tremor in CLD?

A

Alcohol withdrawal.

131
Q

Six signs of decomp. LD?

A
  1. Bruising (coagulopathy)
  2. Ascites
  3. Jaundice
  4. Encephalopathy and altered GCS
  5. Fetor hepaticus
  6. Asterixis
  7. GI bleed evidence (PR)
132
Q

Other causes of low albumin (bar CLD)?

A
  1. Malnutrition
  2. Sepsis
  3. Nephrotic syndrome
  4. Protein losing enteropathy
  5. Acute inflammatory illness
133
Q

Most sensitive marker of liver function?

A

PT. Most specific is ALT.

134
Q

Follow up to raised ALP?

A

ALP isoenzymes

135
Q

Liver US for biliary pathology?

A

Good firstline and good for intrahepatic biliary dilation/gall bladder stones; less good for extrahepatic biliary tree so need MRCP if suspect pathology there (or contrast enhanced CT).

136
Q

Indications for CT in liver disease?

A

Further characterisation of known lesions, staging malignancy, any pancreatic pathology, often biliary pathology, planning or guiding invasive procedures.

137
Q

Indications for liver biopsy?

A
  1. Find aetiology of CLD
  2. Assess stage and severity of liver disease e.g. in NAFLD
  3. Differentiate alcoholic hepatitis from decompensated cirrhosis
  4. Surveillance/response in chronic viral hepatitis.
  5. Serial biopsies are done in AIH; no need in PSC/PBH.
138
Q

Imaging for fibrosis?

A
  1. Fibroscan. US elastography; velocity of wave evaluated. Can assess more of liver parenchyma than biopsy so fewer sampling errors. More acceptable to patients so good for monitoring treatment response (chronic viral hepatitis).
  2. MRI. Standard cross-sectional MRI/CT can show irregularity, nodularity and signs of portal HTN; novel techniques ie diffusion-weighted MR can show early fibrogenesis; MRE (elastography) also useful and, unlike USE, analyses whole liver.
139
Q

Limitations of serum markers/scores for fibrosis?

A

May be low in advanced, stable fibrosis (low inflammation) and can be raised by extrahepatic inflammation.

140
Q

Common causes of abnormal LFTs?

A

Steatosis/steatohepatitis (NAFLD/ALD), viral hepatitis, haemochromatosis, AI LD, drug-induced LD, metabolic (Wilson’s, A1AT), PSC/PBC, multisystemic disease

141
Q

Isolated rise in ALP?

A

Check GGT; if normal then consider non-hepatic; if raised then do US; if bile ducts dilated to MRCP/CT, if focal liver lesion do CT/MRI.

142
Q

Isolated bilirubin rise?

A

Re-check with conjugated; if unconjugated and normal FBC = Gilbert’s

143
Q

Isolated rise in GGT/ALT twice ULN?

A

Assess for RFs (alcohol, metabolic syndrome, medications, viral) and repeat bloods; if ALT still elevated do US abdo (investigate liver lesions/dilated ducts); if none found do liver screen and assess fibrosis. Consider CT/MRCP/biopsy if no obvious cause and still elevated.

144
Q

Non-invasive liver screen components?

A

Serology for viral hepatitis, iron studies, autoantibodie, caeruloplasmin, A1AT, coeliac (TTG).

145
Q

Isolated rise in GGT significance?

A

Rarely indicated significant liver disease.

146
Q

Obstructive jaundice? (aka extrahepatic cholestasis)

A

Most common cause of conjugated hyperbilirubinaemia. Causes inc. gallstones, pancreatic malignancy, cholangiocarcinoma, acute/chronic pancreatitis, LN compression, PSC.

147
Q

Define portal HTN?

A

HVPG >5mmHg. Usually only get Cx above 12mmHg.

148
Q

Signs and symptoms of portal HTN?

A

Varices, ascites, hepatorenal syndrome/SBP, caput medusae, splenomegaly, jaundice, encephalopathy (due to shunts).

149
Q

Diagnosing portal HTN?

A

Gold standard is measuring HVPG by catheterising hepatic vein. Can also be used to determine site of obstruction ie can be post hepatic in Budd-Chiari.

150
Q

Screening for varices?

A

Annually in decomepnsated, 2-3 yearly in compensated, at diagnosis for cirrhosis.

151
Q

Primary prevention varices?

A

NSBB, endoscopic band ligation.

152
Q

Investigating ascites?

A
  1. Bloods: FBC, U&E, CRP, LFT, clotting (amylase, BNP). Urinary sodium.
  2. Abdo US (cirrhosis, HCC, vessel patency)
  3. Paracentesis and fluid analysis (albumin [SAAG], protein, WCC, culture and sensitivites, cytology (malig), amylase, glucose and LDH.
  4. Exclude nephrotic syndrome and cardiac causes
153
Q

Uncomplicated ascites?

A

Not infected or associated with HRS.

154
Q

Diuretics in ascites?

A

Mainstay of treatment but may preclude HRS; need U&E monitoring.

155
Q

Management of refractory ascites?

A

Recurrent paracentesis, TIPSS, transplant.

156
Q

How does portal HTN causes SBP?

A

Splanchnic vasodilation leads to bowel wall oedema and increased permeability therefore get bacterial translocation from gut to ascites.

157
Q

Hyponatraemia in ascites?

A

Decreased circulating volume leads to vasopressin hypersecretion and water retention; get dilutional hyponatraemia.

158
Q

Liver biopsy in ALF?

A

Rarely helpful and high risk due to coagulopathy

159
Q

Mechanism of viral hepatitis?

A

Hep B and C do not cause cell death directly; instead activate immune system leading to inflammation. Can lead to clearance or persistence. Chronic presence leads to waves of inflam/injury/wound healing causing fibrosis/cirrhosis/HCC

160
Q

Mechanism of steatohepatitis?

A

Accumulation of FFA leads to steatosis. Eventually overwhelms hepatocyte homeostasis and get oxidative stress response. Lipid triggers TLR4 causing inflammation (e.g. TNF release) i.e. steatohepatitis and fibrosis. Get swollen hepatocytes ‘ballooning’. See Mallory bodies. Zone 3 particularly effected.

161
Q

How does HBV cause damage?

A

Cytotoxic T cell mediated lysis of infected hepatocytes

162
Q

How does HCV cause damage?

A

Some direct damage; remainder is immune-mediated (upregulate apoptosis/necrosis/angiogenesis) leading to fibrosis.

163
Q

Criteria for super urgent OLT after paracetamol?

A

Any 1 of:

  1. pH <7.25
  2. Lactate >3.5
  3. PT>100 & creatinine >300 & Grade 3/4 HE (or any 2 of these plus life-threatening deterioriation)

CSIM2 (21 decks)

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