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HEPATOLOGY

Signs of portal hypertension Signs of decompensation

●​ Splenomegaly : Cardinal finding ●​ Jaundice
●​ Dilated abdominal wall veins ●​ Ascites / peripheral oedema
●​ Flapping tremor (encephalopathy

●​ Functional unit of liver : Hepatic acinus (SBA)

●​ Cells of immune system - Macrophages (Kupffer cells) (SBA)
●​ Liver stores
○​ Vitamins A, D & B12 in large amounts & vitamin K & folate, are stored in smaller amounts
○​ Iron, copper
●​ Cell types protect against sepsis secondary to translocation of intestinal bacteria : Kupffer
cell (SBA Jan 22)
●​ Main support of liver : Hepatic vein attached with inferior vena cava

Stellate cells / Ito cells

●​ Located in space of Disse (Between hepatocytes & sinusoids)
●​ Functions
○​ Store vitamin A (SBA)
○​ Regulating liver blood flow (SBA)
○​ Immunologically active
○​ Defence against pathogens
○​ Key role in pathology: Development of hepatic fibrosis, precursor of cirrhosis (SBA Jan 23)
○​ Produce endothelin 1 (ET1) > Portal hypertension

24.5 How to identify cause of liver function test (LFT) abnormality ********** SBA

Diagnosis Clinical clue Initial test Additional tests

Alcohol-related AST > ALT; High MCV, IgA

liver disease

NAFLD Metabolic syndrome (central obesity, Ultrasound showing fatty liver

DM, HTN)

Chronic hepatitis B Born in high-prevalence area; HBsAg

injection drug use; blood transfusion

Chronic hepatitis C Injection drug use; blood transfusion HCV antibody HCV-RNA

PBC Itch; raised ALP AMA, Raised IgM

PSC Inflammatory bowel disease MRCP

Autoimmune Other autoimmune diseases ASMA, ANA, LKM, Liver biopsy

hepatitis Raised IgG

Haemochromatosis Diabetes / joint pain / Pigmentation Transferrin saturation, ferritin HFE gene test

Wilson’s disease Neurological signs; haemolysis Ceruloplasmin 24-h urinary copper

Alpha-1-antitrypsin Lung disease α1-antitrypsin level α1-antitrypsin

deficiency genotype

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●​ ALT is considered more specific for hepatocellular damage
●​ Prothrombin time : Provide valuable prognostic information in both acute & chronic liver failure

●​ ↑ ALP & ↑ GGT : Cholestatic liver disease

●​ ↑ ALP & normal GGT : Non hepatic origin (Bone disease / pregnancy)
●​ ↑ GGT & normal ALP : Drugs or NAFLD

●​ Courvoisier’ s Law : If gallbladder is palpable

○​ Jaundice is unlikely to be caused by biliary obstruction due to gallstones
○​ Suggests that jaundice is due to a malignant biliary obstruction (e.g. pancreatic cancer)
●​ Cholangitis is characterised by ‘Charcot’ s triad’ : Jaundice, right upper quadrant pain & fever

⬇️
●​ ↑ Unconjugated bilirubin + Normal Hb, ALT, AST, ALP + USG (N) : Gilbert's syndrome
●​ ↑ Unconjugated bilirubin + ↑ LDH + Hb + Normal ALT, AST, ALP + USG (N) : Hemolysis
●​ ↑ Unconjugated & conjugated bilirubin + ↑↑↑ ALT, AST +/- ↑ ALP + USG (N) : Hepatic jaundice
●​ ↑ Conjugated bilirubin + ↑↑↑ ALP & GGT +/- ↑ ALT, AST + Dilated bile duct on USG : Obstructive /
Post hepatic jaundice

Fig. 24.14 Investigation of jaundice *****

Pre-hepatic jaundice
●​ Isolated bilirubin rise (other
Unconjugated bilirubin ⬆️: Haemolysis screen : (blood film/ reticulocyte
count, haptoglobin, LDH)
LFTs normal) ●​ Positive : Haemolysis work-up including Coombs test
●​ Normal liver ultrasound
●​ Urobilinogen present in urine Conjugated bilirubin ⬆️
●​ Negative : Gilbert syndrome
: Dubin–Johnson & Rotor syndromes (very rare)

Hepatic jaundice ●​ Prothrombin time (severity marker)

●​ Raised conjugated bilirubin / ●​ Aetiology screen:
abnormal enzymes ○​ Acute viral hepatitis serology
●​ No evidence of biliary disease ○​ Autoantibodies / Immunoglobulin
○​ Ceruloplasmin, Iron studies
○​ Consider drug causes, sepsis, congestion

Post-hepatic jaundice ●​ Further imaging (MRCP/CT/EUS)

●​ Raised conjugated bilirubin/
abnormal enzymes
●​ Dilated bile ducts

ACUTE LIVER FAILURE

●​ Cerebral disturbance (hepatic encephalopathy and/or cerebral oedema) : Cardinal manifestation of

acute liver failure (SBA)
●​ Hepatitis B core IgM antibody : Best screening test for acute hepatitis B infection (SBA)
●​ PT : Laboratory test of greatest prognostic value & should be carried out at least twice daily (SBA)

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24.18 Adverse prognostic criteria in acute liver failure1 *****

Paracetamol overdose

●​ pH < 7.25 at or beyond 24 hours following the overdose and after fluid resuscitation Or
●​ Arterial lactate > 5 mmol/L at presentation & > 4 mmol/L 24 hours later after fluid resuscitation Or
●​ PT > 100 s plus encephalopathy grade 3 or 4 plus serum creatinine > 300 µmol/L (≅ 3.38 mg/dL) or anuria

Non-paracetamol cases

●​ Prothrombin time > 100 secs (or INR > 6.5) with any grade of encephalopathy Or
●​ Any three of the following2
○​ Jaundice to encephalopathy time > 7 days
○​ Age < 10 or > 40 year
○​ Bilirubin > 300 µmol/L (≅ 17.6 mg/dL)
○​ Prothrombin time > 50 secs (or INR >3.5)
○​ Unfavourable aetiology, e.g. seronegative hepatitis or idiosyncratic drug reaction

1
Predict a mortality rate of ≥ 90% and are an indication for possible liver transplantation.
2
In the absence of encephalopathy INR > 2 after vitamin K repletion is mandatory.

Feature Prehepatic Jaundice Hepatic Jaundice Posthepatic Jaundice

Bilirubin ⬆️ unconjugated ⬆️ Both ⬆️ conjugated

Urine Color Normal Dark urine Very dark

Stool Color Normal or dark Pale or normal Pale

LFTs Normal ⬆️⬆️⬆️ ALT, AST. ⬆️⬆️⬆️Elevated ALP

Urinary Bilirubin Absent Present

Urinary Urobilinogen Increased Decreased or normal Absent

ASCITES

●​ Splanchnic arterial vasodilation - main factor leading to ascites in cirrhosis mediated by vasodilators
(mainly nitric oxide) (SBA Jan 23)
●​ Measurement of protein concentration & SAAG - To distinguish ascites of different aetiologies
●​ A gradient of > 11 g/L (1.1 g/dL) is 96% predictive that ascites is due to portal hypertension (SBA)
●​ Ascitic amylase > 1000 U/L identities pancreatic ascites (SBA)
●​ Low ascites glucose concentrations suggest malignant disease or tuberculosis
●​ Polymorphonuclear leukocyte > 250×106 /L strongly suggest infection (SBP) (SBA)
●​ Chylous ascites :Triglyceride > 1.1 g/L (110 mg/dL) is diagnostic

⬆️
●​ First line drug : Spironolactone (because it is a powerful aldosterone antagonist) (SBA)
○​ A/E : Painful gynaecomastia & K, in which case amiloride can be substituted (SBA)
●​ First-line treatment of refractory ascites : Large-volume paracentesis (SBA)

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24.22 Causes of ascites **********

Low SAAG (< 11 g/L or 1.1 g/dL) High SAAG (> 11 g/L or 1.1 g/dL)

Common causes

Malignant disease: ●​ Cirrhosis

●​ Hepatic ●​ Cardiac failure
●​ Peritoneal

Other causes

●​ Acute pancreatitis Hepatic venous occlusion:

●​ Lymphatic obstruction ●​ Budd–Chiari syndrome
●​ Infection: Tuberculosis ●​ Sinusoidal obstruction syndrome
●​ Nephrotic syndrome (Veno-occlusive disease)
●​ Protein-losing enteropathy
●​ Severe malnutrition

Rare causes

●​ Hypothyroidism ●​ Constrictive pericarditis

●​ Meigs syndrome

●​ Early Budd–Chiari syndrome : High SAAG & Ascites with high protein content ( > 25 g/L)
●​ Chronic Budd–Chiari syndrome : Protein concentration may fall but SAAG remains elevated
●​ Meigs syndrome
○​ Right pleural effusion with or without ascites & a benign ovarian tumour
○​ The ascites resolves on removal of the tumour
○​ Although usually associated with a low SAAG, it can also be seen with a high SAAG

●​ High SAAG (> 11 g/L or 1.1 g/dL), Low ascitic protein (< 25 g/L (2.5 g/dL) : Cirrhosis
●​ High SAAG (> 11 g/L or 1.1 g/dL), High ascitic protein (> 25 g/L or 2.5 g/dL) : Cardiac failure or hepatic
venous outflow obstruction

𝗦𝗣𝗢𝗡𝗧𝗔𝗡𝗘𝗢𝗨𝗦 𝗕𝗔𝗖𝗧𝗘𝗥𝗜𝗔𝗟 𝗣𝗘𝗥𝗜𝗧𝗢𝗡𝗜𝗧𝗜𝗦 ********** SBA Jan 22,Jul 23

●​ Abdominal pain or fever in a patient with obvious features of cirrhosis & ascites
●​ Diagnostic paracentesis : Cloudy fluid & an ascites neutrophil count of > 250 × 106/L almost
invariably indicates infection (SBA)
●​ Most common organism : Escherichia coli (SBA Jan 22, Jul 23)
●​ Finding of multiple organisms on culture should arouse suspicion of a perforated viscus (SBA)
●​ Rx : Immediate broad-spectrum antibiotics : Cefotaxime or piperacillin / tazobactam (SBA)
●​ Prophylaxis

🔻
○​ Prophylactic antibiotics : Norfloxacin, ciprofloxacin or co-trimoxazole
○​ Primary antibiotic prophylaxis incidence of SBP in patient with low ascitic protein < 15 g/L

HEPATIC ENCEPHALOPATHY **********

●​ Inability to concentrate, delirium, disorientation, drowsiness, slurring of speech & coma

●​ Examination shows
○​ Flapping tremor (asterixis)
○​ Constructional apraxia : Inability to perform simple mental arithmetic tasks or to draw objects
such as a star
○​ Hyper-reflexia, Bilateral extensor plantar responses

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●​ Chronic hepatic encephalopathy / hepatocerebral degeneration
○​ Dementia
○​ Cerebellar dysfunction
○​ Parkinsonian syndromes
○​ Spastic paraplegia
●​ Neurotoxins causing encephalopathy : Ammonia : Most important (SBA)
●​ EEG : Diffuse slowing of normal alpha waves with eventual development of delta waves (SBA)
●​ Rx : Lactulose (osmotic laxative) (SBA)

24.27 Factors precipitating hepatic encephalopathy **********

●​ Drugs (especially sedatives, antidepressants) ●​ Hypokalaemia

●​ Dehydration (including diuretics, paracentesis) ●​ Hyponatraemia
●​ Portosystemic shunting ●​ Constipation
●​ Infection ●​ ↑ Protein load (including gastrointestinal bleeding)

Management of acute variceal bleeding

●​ All patients with cirrhosis & GI bleeding should receive prophylactic broad-spectrum antibiotics (IV
cephalosporin or piperacillin / tazobactam) as treatment with antibiotics improves survival (SBA)
○​ Pharmacological reduction of portal venous pressure : Terlipressin (synthetic vasopressin
analogue) (SBA)
●​ Variceal ligation (‘banding’) : Most widely used initial treatment & is undertaken if possible at time
of diagnostic endoscopy
●​ Primary prevention of variceal bleeding : Non-selective β-blocker (propranolol or nadolol or
Carvedilol) (SBA)
○​ Unable to tolerate or adhere to β-blocker therapy : Prophylactic banding

𝗔𝗰𝘂𝘁𝗲 𝗛𝗕𝗩 𝗶𝗻𝗳𝗲𝗰𝘁𝗶𝗼𝗻 𝗖𝗵𝗿𝗼𝗻𝗶𝗰 𝗛𝗕𝗩 𝗶𝗻𝗳𝗲𝗰𝘁𝗶𝗼𝗻 𝗔𝗰𝘂𝘁𝗲 𝗹𝗶𝘃𝗲𝗿 𝗳𝗮𝗶𝗹𝘂𝗿𝗲 𝗳𝗿𝗼𝗺 𝗵𝗲𝗽𝗮𝘁𝗶𝘁𝗶𝘀 𝗕 /
𝗪𝗶𝗻𝗱𝗼𝘄 𝗽𝗲𝗿𝗶𝗼𝗱

●​ 𝗛𝗕𝘀𝗔𝗴 (+) ●​ 𝗛𝗕𝘀𝗔𝗴 (+) > 6 m ●​ 𝗔𝗻𝘁𝗶-𝗛𝗕𝗰 𝗜𝗴𝗠 (+)

●​ 𝗔𝗻𝘁𝗶-𝗛𝗕𝗰 𝗜𝗴𝗠 (+) ●​ 𝗔𝗻𝘁𝗶-𝗛𝗕𝗰 𝗜𝗴𝗚 (+) ●​ HBsAg (-)

Immunisation 𝘄𝗶𝘁𝗵𝗼𝘂𝘁 𝗶𝗻𝗳𝗲𝗰𝘁𝗶𝗼𝗻 𝗥𝗲𝗰𝗼𝘃𝗲𝗿𝘆 𝗳𝗿𝗼𝗺 𝗶𝗻𝗳𝗲𝗰𝘁𝗶𝗼𝗻 Precore mutation

SBA Jul 24

●​ 𝗔𝗻𝘁𝗶-𝗛𝗕𝘀 (+) ●​ 𝗔𝗻𝘁𝗶-𝗛𝗕𝘀 (+) ●​ High viral load / HBV DNA

●​ Anti-HBc IgG (-) ●​ 𝗔𝗻𝘁𝗶-𝗛𝗕𝗰 𝗜𝗴𝗚 (+) ●​ HBeAg (-)
●​ HBsAg (-) ●​ HBsAg (-)

HBV DNA → HBsAg → HBeAg → Anti-HBc IgM → Anti-HBc IgG → Anti-HBe → Anti-HBs

HBV

●​ Vertical transmission from mother to child in perinatal period : Most common cause of infection &
carries the highest risk of ongoing chronic infection (90%–95%) (SBA)
●​ HBsAg : Main indicator of active infection (SBA)
●​ HBeAg : Part of core Ag that is detectable in blood & used as an indicator of viral replication (SBA)
●​ Viral load : Important in detecting flares of HBeAg (-) hepatitis & monitoring response to antiviral
therapy (SBA)
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●​ Pre-core mutant infection / HBeAg-negative chronic hepatitis (SBA)

○​ Failure of secretion of e antigen into serum
○​ Have high levels of viral production but no detectable e antigen in serum
○​ HBV DNA (+)

HCV

●​ Anti-HCV antibodies : Initial screening test for chronic infection (SBA)

●​ HCV RNA : Can be detected in the blood within 2–4 weeks
○​ Required to confirm active infection (SBA)

Hepatitis E

●​ Most common cause of acute viral hepatitis worldwide

●​ During pregnancy carries a high risk of acute liver failure, which has a high mortality (SBA)

𝗣𝗬𝗢𝗚𝗘𝗡𝗜𝗖 𝗟𝗜𝗩𝗘𝗥 𝗔𝗕𝗦𝗖𝗘𝗦𝗦 ***

High grade fever + RUQ pain + Tender hepatomegaly

●​ Confirmatory : Needle aspiration under ultrasound guidance (SBA)

●​ Abscess caused by gut-derived organisms : Colonoscopy to exclude colorectal carcinoma (SBA)

Management
●​ Combination of antibiotics, such as ampicillin, gentamicin and metronidazole (SBA)

Liver abscess due to anaerobic bacteria (Bacteroides, Streptococcus bovis) >>> Do colonoscopy

NAFLD

Obesity / ⬆️BMI + DM + HTN + ⬆️ALT,AST +Bright liver on USG

●​ Liver biopsy : Gold standard (SBA)
○​ NASH with a mainly centrilobular, acinar zone 3 distribution
○​ Perisinusoidal fibrosis is a characteristic feature of NAFLD (SBA)
●​ Sustained weight reduction - associated with significant improvement in histological & biochemical
NASH severity (SBA Jul 22)

𝗔𝗨𝗧𝗢𝗜𝗠𝗠𝗨𝗡𝗘 𝗛𝗘𝗣𝗔𝗧𝗜𝗧𝗜𝗦 ***** SBA Jan 22

H/O autoimmune disease + ↑ ALT, AST + ↑ IgG + (+) ANA, ASMA

●​ Elevated serum IgG levels are an important diagnostic & treatment response (SBA Jan 22)
●​ Liver biopsy : To confirm diagnosis & to stage any liver fibrosis (SBA) - Interface hepatitis
●​ Treatment : Glucocorticoids is life-saving (SBA)
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PRIMARY BILIARY CHOLANGITIS **********

PBC : AMA, IgM, HLA-DR8

Middle aged woman + Severe fatigue & itching + Hyperpigmentation + H/O Autoimmune disease
(Sjogren's syndrome / thyroid disease) + Cholestatic LFTs (↑ ALP) + AMA (+)

●​ Strongly associated with antimitochondrial antibodies (AMA) which in combination with cholestatic
liver enzymes are diagnostic of PBC (SBA)
●​ Genetic association with HLA-DR8 (SBA)
●​ Investigation : Antimitochondrial antibodies (AMA)
●​ Optimal first-line treatment : Ursodeoxycholic acid (UDCA) (SBA)
●​ Pruritus
○​ Due to up-regulation of opioid receptors & increased levels of endogenous opioids (SBA)
○​ First-line treatment : Anion-binding resin cholestyramine (SBA)

PRIMARY SCLEROSING CHOLANGITIS **********

Young + Fatigue & itching + Bloody diarrhea / UC + ↑ ALP >>> Do MRCP

●​ Treatment : UDCA may have benefit in terms of reducing colon carcinoma risk (SBA)
●​ Leading cause of death in PSC : Cholangiocarcinoma (SBA)
●​ Patients with PSC & colitis should undergo annual colonoscopy for colorectal cancer (SBA)

ALD NAFLD AIH PBC PSC

History Alcohol DM, HTN, ↑ BMI Autoimmune disease UC

Symptoms Asymptomatic Anorexia, abdominal pain, Fatigue, Pruritus

arthralgia, Jaundice

Investigation

CBC ↑ MCV

Hepatitic Cholestatic
LFTS
↑ AST > ALT, GGT ↑ ALT, AST, GGT ↑ ALT, AST ↑ ALP, GGT

Ig ↑ IgA ↑ IgG ↑ IgM

Ab ASMA, Anti-LKM, Anti-SLA AMA p-ANCA

Confirmatory Liver biopsy Liver biopsy AMA MRCP

Perisinusoidal fibrosis Interface hepatitis

Rx Alcohol cessation Weight reduction Glucocorticoid UDCA,

Cholestyramine

Complications
●​ Cirrhosis of liver in all cases
●​ PSC : ↑ Gall bladder Ca, Colon Ca, cholangiocarcinoma

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24.54 Comparison of PBC & PSC **********

PBC PSC

Gender (F : M) 9:1 1:3

Age Older: median age 50–55 years Younger: median age 20–40 years

Disease Autoimmune disease (e.g. Sjögren syndrome, thyroid Ulcerative colitis

associations disease)

Autoantibody 90% AMA +ve pANCA +ve

(non-specific & not diagnostic)

Predominant Intrahepatic Extrahepatic > intrahepatic

bile-duct injury

HCC

H/O CLD + Deterioration of ascites, LFTs + Weight loss

●​ Alpha-fetoprotein (AFP) : Useful biomarker of disease progression or response to treatment (SBA)

●​ Confirmatory : Multi-phase contrast-enhanced CT or MRI (SBA)

𝗗𝗥𝗨𝗚 𝗜𝗡𝗗𝗨𝗖𝗘𝗗 𝗟𝗜𝗩𝗘𝗥 𝗜𝗡𝗝𝗨𝗥𝗬

●​ Most common picture is a mixed cholestatic hepatitis

●​ Co-amoxiclav : Most common antibiotic to cause abnormal LFTs (SBA)

𝗚𝗘𝗡𝗘𝗧𝗜𝗖 𝗛𝗔𝗘𝗠𝗢𝗖𝗛𝗥𝗢𝗠𝗔𝗧𝗢𝗦𝗜𝗦 ********** SBA Jan 21

Features of DM (Polyuria, ↑ thirst, ↑ Blood glucose) + Pigmented skin +/- Heart failure / Joint pain /
Chondrocalcinosis / pseudogout / Infertility / Loss of libido + Abnormal LFTs

●​ Hormone hepcidin inhibits iron transport by binding to ferroportin on enterocytes & macrophages
●​ (~ 90%) Homozygous single point mutation on chromosome 6 > Cysteine to tyrosine substitution at
position 282 (C282Y) in HFE protein > ↓ Plasma hepcidin > Uncontrolled ↑ iron absorption (SBA)
●​ Serum ferritin : Screening test for iron overload (SBA)
●​ ↑ Ferritin & ↑ transferrin saturations ( > 40% in women, > 50% in men) : Prompt molecular
testing for HFE mutations (SBA)
●​ GH is suspected but HFE genotyping is normal : MRI liver or liver biopsy
●​ First-degree family members should be investigated, preferably by genetic screening (SBA Jan 21)
●​ Treatment : Weekly venesection of 500 mL blood (250 mg iron) (SBA)
●​ Screening for hepatocellular carcinoma is mandatory because this is the main cause of death (SBA)

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𝗪𝗜𝗟𝗦𝗢𝗡’𝗦 𝗗𝗜𝗦𝗘𝗔𝗦𝗘 (𝗵𝗲𝗽𝗮𝘁𝗼𝗹𝗲𝗻𝘁𝗶𝗰𝘂𝗹𝗮𝗿 𝗱𝗲𝗴𝗲𝗻𝗲𝗿𝗮𝘁𝗶𝗼𝗻) ********** SBA Jan 22, Sept 21

Young patient + Recurrent hepatitis / CLD / Abnormal movements / dementia / Psychiatric signs +
Hemolysis + +/- KF ring (Greenish-brown discoloration of corneal margin)

●​ Autosomal recessive disorder of Cu metabolism

●​ Caused by mutations in ATP7B gene on chromosome 13 (SBA)
●​ ATP7B gene encodes a transmembrane copper-transporting ATPase which excretes copper into
bile & loss of function causes excessive copper accumulation
●​ WD should be considered in any patient under the age of 40 presenting with recurrent acute
hepatitis or CLD of unknown cause especially when accompanied by haemolytic anaemia
●​ Kayser–Fleischer rings
○​ Pathognomonic sign / Most important single clinical clue to diagnosis (SBA Jan 22)
○​ Golden / Greenish-brown discoloration of corneal margin appearing first at upper periphery
then develops inferiorly & ultimately becomes circumferential
●​ Low serum ceruloplasmin : Best single laboratory clue to the diagnosis (SBA)
●​ Confirmatory: Measuring 24-h urinary copper excretion while giving D-penicillamine (SBA Sept 21)
●​ Treatment : Copper-binding agent penicillamine is the drug of choice (SBA)

ALPHA-1- ANTITRYPSIN DEFICIENCY

Young / Middle aged + No significant smoking history + Early onset COPD / EMPHYSEMA

●​ Alpha-1-antitrypsin (α1-AT) is produced by liver

●​ A serine protease inhibitor, mainly inhibits neutrophil elastase in lungs (SBA)

⬇️
●​ Lung Pathogenesis: Uncontrolled neutrophil elastase activity
●​ Absence or AAT > Neutrophil elastase destroys alveolar walls > Panacinar emphysema
specially in lower lobes
●​ Diagnosis is made from low plasma α1-AT concentration & genotyping for the presence of mutation
●​ Liver histology: Accumulation of periodic acid–Schiff-positive granules within individual hepatocyte
●​ Risk of severe & early-onset emphysema means that all patients should stop smoking (SBA)

GILBERT SYNDROME**********

⬆️ unconjugated
H/O physical stress (Intercurrent illness / Fasting / Exercise / Blood donation / Pregnancy) +
bilirubin + Other LFTs, CBC with PBF, LDH, Reticulocyte : Normal + No bilirubinuria

●​ Most common inherited disorder of bilirubin metabolism

●​ Autosomal recessive trait when caused by mutation in promoter region of gene for UDP-glucuronyl
transferase enzyme (UGT1A1) (SBA)
●​ Not associated with liver injury & has an excellent prognosis
●​ Needs no treatment

BUDD CHIARI SYNDROME **********

H/O prothrombotic conditions (Polycythemia / PNH / Pregnancy) +

Sudden onset of upper abdominal pain, ascites & tender hepatomegaly

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●​ Doppler ultrasound : Obliteration of hepatic veins & reversed flow or associated thrombosis in
portal vein (SBA)
●​ CT may show enlargement of caudate lobe (SBA)

ACUTE FATTY LIVER OF PREGNANCY ***** SBA

3rd trimester + Abdominal pain & vomiting + Hepatitic LFTs ( ↑ ALT, AST)

●​ Management : Supportive care & by delivery of foetus

HELLP syndrome ***** SBA

Pregnancy + Hemolysis (↓ Hb, ↑ LDH, Schistocytes) + ↓ Platelet + Abnormal LFTs

OBSTETRIC CHOLESTASIS ***** SBA

3rd trimester + Pruritus + Cholestatic LFTs (↑ ALP, GGT)

●​ Due in part to the cholestatic effect of high oestrogen levels

●​ Treatment : Ursodeoxycholic acid (UDCA)

24.57 Examples of common causes of drug-induced hepatotoxicity ********** SBA / MCQ

Pattern Drug Pattern Drug

Cholestasis ●​ Chlorpromazine Venous outflow ●​ Busulfan

●​ High-dose oestrogens obstruction ●​ Azathioprine
●​ Alkylating agents

Cholestatic ●​ Co-amoxiclav Hepatocyte ●​ Paracetamol

hepatitis ●​ Flucloxacillin necrosis ●​ Diclofenac
●​ Chlorpromazine ●​ Isoniazid
●​ Statins ●​ Herbal remedies
●​ NSAIDs ●​ Cocaine
●​ Anabolic steroid ●​ Ecstasy

Acute hepatitis ●​ Rifampicin Autoimmune ●​ Nitrofurantoin

●​ Isoniazid hepatitis-like ●​ Checkpoint inhibitors (nivolumab
●​ Cocaine, Ecstasy / pembrolizumab)

Microvesicular ●​ Tetracycline Macrovesicular ●​ Tamoxifen

steatosis ●​ Sodium valproate steatosis ●​ Amiodarone

NASH ●​ Amiodarone Portal HTN ●​ Chronic overdose of vitamin A

Fibrosis ●​ Methotrexate Granuloma ●​ Allopurinol

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