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HPB Flashcards

1
Q

Liver can be divided into how many hemi-livers and how many main sections?

A

2 hemi-liver and 4 main sections

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2
Q

Liver can be divided into how many functional segments based on independent vascular flow and biliary drainage?

A

8!
Divided by 1 transverse plane and 3 sagittal planes

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3
Q

Blood supply of liver?

A

Portal vein 75%, hepatic artery proper 25%
Portal vein is from splenic vein and SMV

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4
Q

3 main hepatic veins?

A

Right Hepatic Vein - Drain Segment 5-8
Middle Hepatic vein - Drain segment 4, 5, 8
Left hepatic vein - drain segment 2 and 3

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5
Q

Metabolic functions of liver?

A

Glycogenesis, Glycogenolysis
Gluconeogenesis
Lipogenesis, Lipolysis
Vit D activation
Detoxification
Vitamin, iron, copper storage
Phagocytosis

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6
Q

How to investigate portal HTN?

A

US Liver and Spleen -
Dilated splenic and SMV
Splenomegaly
Dilated Portal vein
Porto-systemic collaterals
Reduced portal flow mean velocity
Others - Ascites, nodular liver etc

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7
Q

Choice of diuretic to treat ascites in patients with liver disease?

A

Spironolactone - aldosterone antagonist.

Renal hypoperfusion stimulates RAAS in ascites pathogenesis.

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8
Q

Presentation of ascites?

A

Progressive abdominal distension with discomfort
Weight gain, SOB, dyspnoea, early satiety
Fever, abdominal tenderness, Altered mental status

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9
Q

What is SAAG?

A

Serum-ascites albumin gradient.
Correlates directly with portal pressure. SAAG above 1.1g/dL means portal HTN

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10
Q

Imaging for ascites?

A

Chest XR - assess for pleural effusion. Diaphragmatic channel opens up and transmits fluid.
US / CT for liver and spleen

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11
Q

Biochemical test for ascites?

A

FBC, LFT, U/E/Cr

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12
Q

What pathos can cause high AST specifically?

A

Myocardial Infarction
Muscle damage

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13
Q

AST/ALT ratio <1 means?

A

Uncomplicated viral hepatitis
Minor fatty liver disease
Extrahepatic cholestasis

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14
Q

AST/ALT>1 means?

A

Alcoholic hepatitis (AST/ALT >2)
Decompensated cirrhosis
HCC, liver mets
Muscle damage
Myocardial infarction
Fulminant, necrotic hepatitis

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15
Q

Cholestasis shows high biochemical markers?

A

ALP, GGT

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16
Q

High ALP means?

A

Cholestasis (obstructive or non-obstructive)
Seminoma
3rd trimester of pregnancy
Chronic Kidney disease
High osteoblast activity
Infiltrative disease of liver e.g. malignancies

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17
Q

What does GGT show

A

Cholestasis
Alcohol use

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18
Q

INR significance?

A

1.1 or below considered normal.
INR between 2.0 to 3.0 is considered effective therapeutic range for patients taking warfarin.

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19
Q

What is focal nodular hyperplasia?

A

Benign tumour characterized by central stellate scar

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20
Q

How much albumin to give in therapeutic Paracentesis for ascites?

A

8g IV for every 1L of ascitic fluid drained.
Albumin prevents paracentesis-induced circulatory dysfunction with risk of hypotension/recurrent ascites/HRS/death

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21
Q

What is haemochromatosis?

A

iron-binding protein accumulates in various tissues, typically leading to liver damage, diabetes mellitus, and bronze discoloration of the skin.

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22
Q

Peripheral signs of chronic Liver disease?

A

Gynaecomastia
Clubbing, pallor
Palmar erythema
Pedal edema
Flapping tremor
Scleral icterus
Scratch marks

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23
Q

What is liver haemangioma?

A

Benign vascular lesions with hamartomatous outgrowths of endothelium made of widened blood vessels rather than true neoplasms. Some tumours express estrogen receptors.

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24
Q

Presentation of liver haemangioma?

A

Usually asymptomatic, found incidentally
Pain from liver capsule stretch - non specific upper abdo fullness or vague abdo pain
Mass effects from compressing
CCF from large AV shunt

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25
Q

1st line to investigate liver haemangioma?

A

US 1st choice. Accuracy 70-80%.
Well-circumscribed, homogenous, hyperechoic lesion.

Dont biopsy cuz risk of huge haemorrhage

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26
Q

How does liver haemangioma show on CT?

A

Triphasic CT
Peripheral enhancement in arterial phase, centripetal filling on portal venous phase.
Retention of contrast on delayed phase.

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27
Q

How to treat liver haemangioma?

A

Mostly treated safety with observation. Surgical removal for symptomatic or complicated

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28
Q

Diagnosis of acute pancreatitis?

A

**MUST FULFIL 2/3:
**1. Abdo pain with epigastric pain
2. Serum lipase / amylase at least 3x higher
3. Characteristic findings on CECT, MRI or US

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29
Q

What causes death in acute pancreatitis?

A

Early - due to organ failure
Late - infected pancreatic necrosis with resultant sepsis and multi-organ failure

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30
Q

2 commonest causes of acute pancreatitis?

A

Gallstones and alcohol. 60-80% of casess

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31
Q

Pathophysiology of acute pancreatitis - auto digestion?

A

Unregulated activation of trypsin within pancreatic acinar cells. Pro-enzymes activated causing auto-digestion.

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32
Q

Pathophysiology of acute pancreatitis - gallstones?

A

Obstructed pancreatic duct causing higher pressure in pancreatic duct
Extravasation of pancreatic juice leading to injury of gland.

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33
Q

Pathophysiology of acute pancreatitis - interstitial edema due to gallstone blockage?

A

Impaired blood flow to cells causing ischaemic cellular injury.
Proenzymes activated causing pancreatic acinar cell damage.

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34
Q

Which body posture alleviates acute pancreatitis pain?

A

Sitting up and leaning forward

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35
Q

Normal serum amylase level?

A

30-100U/L
Levels rise within a few hrs but normalize in 5 days
Elevation for >10 days indicate complications like pseudocysts

Can miss later presentations of pancreatitis

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36
Q

Normal Serum lipase level?

A

10-140 U/L
Levels rise within 4-8 hrs and stay elevated for 8-14 days

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37
Q

How to use C-Reactive Protein levels?

A

Risk stratification for acute pancreatitis.
>150mg/L within 48 hrs a/w severe pancreatitis

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38
Q

Where is CEA elevated?

A

Most adenoCAs.
CRC, pancreatic, breast, lung, gastric, cholangio, endometrial, medullary thyroid
Others: IBD, Pancreatitis, Hepatitis

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39
Q

Early local complication of acute pancreatitis?

A

Acute peripancreatic fluid collection - Due to increased vascular permeability.
Acute necrotic collection - 30% develop secondary bacterial infection - Enteric GNR

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40
Q

How to tell if acute necrotic collection is sterile or infected?

A

Infected if have gas bubbles on CT / persistent sepsis / progressive clinical deterioration.
Positive culture can be obtained from FNA or during drainage procedure

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41
Q

Late local complication of acute pancreatitis? > 4 weeks

A

Pancreatic pseudocyst.
Presents as persistent pain, mass on exam, persistent high amylase or lipase

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42
Q

3 signs of haemorrhagic pancreatitis?

A

Grey-turner sign - flank ecchymosis
Cullen’s sign - periumbilical ecchymosis
Fox’s sign - inguinal ecchymosis

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43
Q

Complications of pseudocyst

A

Fistula formation
Hemorrhage
Rupture - pancreatic ascites
Obstruction - intestinal, vascular, biliary, gastric outlet
Infection - abscess

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44
Q

Are serum amylase and lipase useful in chronic pancreatitis?

A

No. Commonly normal cuz significant fibrosis causing lower abundance of these enzymes within pancreas.

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45
Q

Whipple procedure?

A

En-bloc removal of distal segment of stomach, DDM, proximal 15cm of JJM, HOP, common BD, Gallbladder.
Pancreatic and biliary anastomosis placed 45-60cm proximal to gastrojejunostomy.
Pancreas and DDM share same arterial supply - gastroduodenal artery. Hence both must be removed.

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46
Q

Commonest pancreatic CA?

A

Ductal adenoCA.
Others include adenosquamous CA, SCC, Acinar cell CA.

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47
Q

Presentation of pancreatic CA?

A

Vague epigastric discomfort and presence of constitutional symptoms despite normal upper endoscopy should prompt further investigations.

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48
Q

Symptoms and signs of pancreatic CA?

A

Classical Courvoisier sign
Obstructive jaundice with pain
New onset DM in elderly patients
Signs of malabsorption
N/V
LOW, anorexia
Upper BGIT

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49
Q

Signs of advanced malignancy in pancreatic CA?

A

Malignant pleural effusion
Virchow’s Node
Trousseau sign of malignancy
Sister Mary Joseph Nodule
Hepatomegaly
Nonbacterial thrombotic endocarditis

Must differentiate Trousseau from in hypoCa

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50
Q

Important test for Pancreatic CA?

A

Carbohydrate Antigen 19-9 (CA19-9)
Can act as prognostic marker - lower the better.
Poor sensitivity and specificity.

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51
Q

CA19-9 elevated in which pathos?

A

Lung CA, Gastric CA, CRC, biliary tract CA, urothelial CA
Pancreatitis, hepatitis, thyroiditis, biliary obstruction

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52
Q

What can be seen in transabdominal US in pancreas stuff?

A

CBD dilatation >7mm, >10mm in post-chole patients
Pancreatic duct dilatation >2mm
Above are worrying signs.
Transabdominal US is first line in jaundiced pt cuz higher sensitivity for determining cholelithiasis over CT

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53
Q

Commonest staging modality for pancreatic CA?

A

Tri-phasic “Pancreatic protocol CT scan” and CT thorax

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54
Q

What is double duct sign in CT for pancreatic CA?

A

Simultaneous dilatation of CBD (intra-pancreatic segment) and pancreatic duct

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55
Q

Reason for ERCP stenting post-op in acute pancreatic CA?

A

Relieve biliary obstruction. BUT raise risk of post-op complications in patients with resectable disease

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56
Q

Pylorus-preserving Pancreatico-duodenectomy Resection - PPPDR?

A

Preserve gastric antrum, pylorus, proximal DDM - DDM transected at least 2cm distal to pylorus.

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57
Q

Signs of chronic liver disease on PE?

A

Gynaecomastia, clubbing, palmar erythema, flapping tremor of hands
Pruritic scratch marks
Coagulopathy
Chronic alcoholism signs - parotidomegaly, Dupuytren’s contractures
Spider naevi, caput medusa
Distension, scars, hepatomegaly
DRE - pale stools

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58
Q

Courvoisier’s law?

A

When CBD is blocked by stone, GB is rarely distended.
When duct is blocked for some other reason, distension is common.
Gallstones cause obstruction in an intermittent fashion

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59
Q

Commonest causes of obstructive jaundice?

A

Gallstones
Tumour
Hepatitis

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60
Q

Painful obstructive jaundice causes

A

Gallstones, strictures, hepatic causes

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61
Q

Painless obstructive jaundice causes

A

Periampullary tumour

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62
Q

What is periampullary tumour?

A

Tumours that arise within 2cm of ampulla of vater in DDM. Malignancy is suspected when patient is old, jaundice is new onset, PAINLESS AND PROGRESSIVELY WORSENING

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63
Q

Pain comes in which stage of pancreatic CA? Consistency of pain?

A

Pain is a late symptom of pancreatic CA.
Constant and relentless compared to biliary colic which subsides after a few hours.

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64
Q

Pain comes in which stage of pancreatic CA? Consistency of pain?

A

Pain is a late symptom of pancreatic CA.
Constant and relentless compared to biliary colic which subsides after a few hours.

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65
Q

Relevant Hx for pancreatic head CA?

A

New onset DM/Recalcitrant CA.
Dull aching pain radiating to back
Pseudo Gastric outlet obstruction - duodenal obstruction
Worsening steatorrhea

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66
Q

AST / ALT ratio of >2:1 indicates?

A

Alcoholic liver disease

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67
Q

Management option for jaundice?

A

ERCP - use of upper endoscopy and fluoroscopy to evaluate biliary system.

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68
Q

Therapeutic use of ERCP?

A

Removal of common duct stones with sphincterotomy and/or relief of biliary obstruction with biliary stent.

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69
Q

Diagnostic use of ERCP?

A

Brushing, biopsy, FNAC for malignancy

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70
Q

Types of gallstones?

A

Cholesterol stone 85%
Pigment stones 15%

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71
Q

5Fs in cholesterol gallstones

A

Fertility
Female
Fat
Forty
Family hx

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72
Q

Difference between cholesterol and pigment stones

A

Black, sterile, hard, Radiolucent = Cholesterol stone
Brown, infected, soft, Radio-opaque = Pigment stones

73
Q

What posture must u ask pt to do if u see abdominal scar?

A

Tilt head forward. This will reveal incisional hernia.

74
Q

Where does gallstone pain radiate to?

A

Inferior angle of scapula or tip of right shoulder

75
Q

Timing of gallstone pain?

A

Distinct attacks lasting 30 mins to several hours.
Often resolve by 6hrs. If not then suspect complications.

76
Q

What is decompensated cirrhosis?

A

Development of ascites, HE, GI Bleeding.
Poor survival rate unless transplant.

77
Q

How to classify COMPLICATED CHOLELITHIASIS?

A

By organ!
In GB, Common BD, in Gut

78
Q

Complicated gallstone in GB?

A

Hydrops of GB
Acute calculous cholecystitis - leading to acute gangrenous cholecystitis, empyema, porcelain GB, chronic cholecystitis.
Eventually lead to higher risk of GB CA

79
Q

Complicated gallstone in common bile duct?

A

Choledocholithiasis - causing:
- Obstructive jaundice
- Ascending cholangitis
- Secondary biliary cirrhosis
- Gallstone pancreatitis.

80
Q

Indications for gallstone surgery?

A

High risk of malignancy - GB polyp >1cm / stone >2.5cm / porcelain GB
Chronic haemolytic disease e.g. sickle cell, thalassemia.
Relative - elderly with diabetes

81
Q

What % of patients still have abdo pain post-cholecystectomy?

A

10-41%

82
Q

What technique for Lap Cholecystectomy?

A

Hasson Open Technique.
3x 5mm ports inserted in subxiphoid, right subcostal area and right flank.

83
Q

How does gallstone or biliary sludge cause acute cholecystitis?

A

Block cystic duct -> high intraluminal pressure within GB -> compromise blood flow and lymphatic drainage within GB wall.
Mucosal ischemia and necrosis results.

84
Q

Are cultures from GB in cholecystitis sterile?

A

Initially sterile, but eventually secondary bacterial infection with enteric organism can occur.

85
Q

History of acute calculous Cholecystitis?

A

Constant, unremitting severe RHC pain. Due to inflammation spreading to parietal peritoneum.
Hx of fatty food consumption before pain
Radiate to inferior angle of scapula/back/shoulder.

A/w Fever, anorexia, N/V

86
Q

What signs in abdomen can be seen in acute calculous cholecystitis?

A

RHC tenderness with guarding
Murphy’s sign
Palpable GB (30%)

87
Q

Radiological findings of calculous cholecystitis?

A

US HBS 1st line.
Thickened GB wall with edema.
Contracted GB.

88
Q

What is elevated in acute cholecystitis blood test?

A

TW>18 means need to consider complications.
High CRP - consider complicated Gallstone disease
High ALP in LFT.
U/E/Cr - dehydration.
High amylase

89
Q

Empirical IV Abx for acute calculous cholecystitis?

A

Ceftriaxone and metronidazole.

90
Q

Common organisms for infection in acute calculous cholecystitis?

A

E. Coli
Klebsiella
Pseudomonas
Enterococcus

91
Q

Conservative management for calculous cholecystitis?

A

Monitor vitals and resuscitate if needed
Septic workup
Analgesia
Empirical IV Abx

92
Q

Lap cholecystectomy options?

A

Early LC preferred to late LC.
LC avoided for patients beyond 7-10 days from symptom onset unless symptoms suggestive of peritonitis or sepsis.

93
Q

Immediate treatment for acute calculous cholecystectony?

A

Percutaneous cholecystectomy for those not fit for surgery.
E.g. early surg hard due to extensive inflamm or gangrenous GB with thin wall

94
Q

Complications of cholecystectomy?

A

Hydrops
Empyema
Cholecystoenteric fistula
Gangrene and perforation
Emphysematous cholecystitis
Gallstone ileus

95
Q

Primary pathology of acute Acalculous cholecystitis?

A

GB distension with bile stasis and ischemia

96
Q

Risk factors for acalculous cholecystitis?

A

Prolonged ICU stay
Sepsis with hypotension
Extensive burns / multiple trauma
Patients on total PO nutrition - cause biliary stasis

97
Q

Clinical presentation of acalculous cholecystitis?

A

Insidious onset - GB necrosis, gangrene and perforation are frequent at time of diagnosis
Higher rates of gangrenous cholecystitis as compared to gallstone induced AC.

98
Q

What proportion of cholecystectomy patients have choledocholithiasis?

A

5-20% at time of surgery

99
Q

Biochemical markers for CBD gallstones?

A

FBC - leukocytosis with left shift. Can suggest cholangitis.
U/E/Cr - dehydration
LFTs - ALT/AST elevated in early biliary blockage.
Later on, ALP/Serum bilirubin. GGT more elevated than AST/ALT (cholestatic pattern)
High Serum amylase.

100
Q

PE of CBD gallstones?

A

Septic looking, jaundice
Vitals - febrile, hypotension
Abdomen - RUQ/epigastric tenderness
Palpable GB.

101
Q

2 approaches to gallstones in CBD?

A

ERCP Sphincterotomy + stone removal
CBD Exploration (CBDE) (for those unfit for ERCP / failed endoscopic removal)
Generally we try to clear CBD stones via ERCP and proceed with laparoscopic cholecystectomy.

102
Q

What is Mirizzi’s syndrome?

A

Common hepatic duct obstruction secondary to extrinsic compression from an impacted gallstone in cystic duct or infundibulum of GB

103
Q

Charcot’s TRIAD OF CHOLANGITIS?

A

FEVER
JAUNDICE
RUQ PAIN

104
Q

HOW DO BACTERIA ENTER BILE AND BILIARY TRACT IN CHOLANGITIS?

A

IN OBSTRUCTION, THERE IS RISE IN BILIARY DUCTAL PRESSURE WHICH LEADS TO BACTERIA ENTERING CIRCULATION SYSTEM VIA CHOLANGIO-VENOUS REFLUX.
NORMAL BARRIER MECHANISMS LIKE SPHINCTER OF ODDI OR FLUSHING ACTION OF BILE IS DISRUPTED.

105
Q

Additional 2 criteria for Reynold’s Triad in Cholangitis?

A

Hypotension
Altered mental state

106
Q

Management goals of cholangitis?

A

Treat biliary infection and obstruction
Resuscitate if have septic shock.
Consider Emergent biliary decompression with ERCP.

107
Q

What empirical Abx for cholangitis?

A

IV Ceftriaxone and metronidazole. Imipenem if patient is in shock

108
Q

Risk factors for GB CA?

A

Cholelithiasis. Larger and symptomatic stones a/w higher risk
Calcified GB
GB polyps
Others

109
Q

Clinical presentation of GB CA?

A

Asymptomatic - incidental histological finding after cholecystectomy.
Early - mimic gallstone inflamm
Late - biliary and stomach obstruction

110
Q

US signs for GB CA?

A

US - thickened irregular GB wall or mass replacing GB with invasion of liver.
Doppler signal in GB mass.
Enlarged LNs
Dilated biliary tree

111
Q

CTAP uses for GB CA?

A

Needed for staging, assessment of local invasion but poor for nodal spread. Hence do prior to definitive surgery.

112
Q

MRCP uses for GB CA?

A

Allows complete assessment of biliary, vascular, nodal, hepatic and adjacent organ involvement

113
Q

1 stage vs 2 stage cholecystectomy for GB CA?

A

1 stage: chole with intraoperative frozen section KIV extended chole w/wo hepatectomy
2 stage: simple chole then wait for histo to guide further management

114
Q

Commonest cholangioCA?

A

AdenoCA

115
Q

Risk factors for cholangioCA?

A

Chronic cholestasis - causing prolonged inflamm of biliary epithelium.
Congenital biliary tract disorders
DM

116
Q

Clinical Presentation of cholangioCA?

A

Intrahepatic - non specific symptoms
Extrahepatic -
painless progressive obstructive jaundice
Dark urine, pale stools, pruritus
LOW/LOA
Malaise, fatigue, night sweats

117
Q

PE of cholangioCA?

A

Jaundice (90%)
Hepatomegaly (25-40%)
RUQ mass (10%)
Fever (2-14%)
RUQ tenderness

118
Q

Classification of cholangioCA?

A

A few ways. Anatomical location - INTRAHEPATIC (5-10%) vs HILAR (60-70%) vs EXTRAHEPATIC (20-30%)

119
Q

Classification for hilar lesions in cholangioCA?

A

Bismuth Corlette Classification.
Type 1: below confluence of hepatic ducts
2: Tumour reaching confluence
3: Involves CHD and either left or right HD
4: Multicentric or involving confluence with both Hepatic Ducts

120
Q

Biochemical tests for cholangioCA?

A

FBC/RP/PT, INR, APTT
LFT - non specific rise in serum BRB, high ALP + GGT
High C19-9
High CEA

121
Q

US findings for cholangioCA? (first line)

A

US HBS - first line. Check biliary duct dilatation. Can localize site of obstruction

122
Q

Imaging options for cholangioCA?

A

US HBS
CT triphasic
Cholangiography (MRCP / ERCP)
Endoscopic US with FNA
PET-CT

123
Q

Prognosis of cholangioCA?

A

Most patients have unresectable disease at presentation and die within a year.
5 year survival rates post surgeries is like 50% max.

124
Q

Management option for cholangioCA?

A

Complete surgical resection with histologically negative margins is only cure.
Only 25% of tumours are resectable.
No proven role for adjuvant chemo or radiotherapy.

125
Q

Criteria for unresectability of hilar lesions?

A

Vascular involvement
Extent of distant spread
Extent of local disease

126
Q

Management options for pancreatic CA?

A

Chemo and Radiotherapy.
Surgery with curative resection.

127
Q

When is HCC mostly diagnosed?

A

In 5th and 6th decade

128
Q

Risk factors for HCC?

A

CLD, HBV/HCV infection, cirrhosis (alcoholic and non-alcoholic)

129
Q

Molecular classification for HCC?

A

Proliferative class - HBV, high tumour grade, high AFP, worse prognosis
Non-proliferative class - HCV, alcohol, low tumour grade, low freq of vascular invasion, better prognosis

130
Q

Histological subtypes of HCC?

A

Non-fibrolamellar - a/w/ HBV, Cirrhosis
Fibrolamellar - a/w younger patients, equal gender distribution, not a/w cirrhosis or HBV. 70% resectable. Better prognosis

131
Q

Gold standard for HCC imaging?

A

Triphasic CT Scan

132
Q

What to investigate for in HCC after confirming HCC?

A

Stage disease, mainly with CT scan and assess tumour burden
Assess liver function
Check for complications of disease and for pre-operative assessment.

133
Q

Radiological hallmark between HCC and haemangioma?

A

HCC mets shows portal venous enhancement
Haemangioma shows capsular enhancement in delayed phase.

134
Q

Which vessel does HCC invade most commonly?

A

Portal vein.
Can show enhancing portal vein thrombus.

135
Q

How to assess liver function for staging of HCC?

A

Biochemical tests -> Child-Pugh score
Indocyanine green assessment (ICG)
CT volumetry/MR volumetry

136
Q

Child-Pugh Score?

A

Albumin (1-3 points each)
Bilirubin
Coagulation (PT time)
Distension (ascites)
Encephalopathy

5-6 points = Class A. Well-compensated disease. 100/85%
7-9 points = Class B. Strong functional compromise. 80/60%
10-15 points = Decompensated. Not for resection. 45/35%.
These classes correlate with 1-yr and 2-yr patient survival.

137
Q

How to use ICG assessment for HCC?

Indocyanine green

A

Assess adequacy of post-resection hepatic function.
Assess % of ICG left in liver after 15 minutes. Shows liver function. Normal liver should have less than 10% left

138
Q

What is CT volumetry / MR volumetry used for in HCC?

A

To assess Future Liver Remnant (FLR).
FLR : Standard Liver volume ratio is used as indicator to predict post-op liver failure.
Normally FLR above 20%.
Cirrhotic liver has FLR above 40-50% of SLV

139
Q

How to assess patient’s performance status in HCC?

A

ECOG performance scale
4 means ADL dependent and totally confined to bed/ chair

140
Q

Curative treatment modality for HCC management?

A

Curative:
surgical resection +- ablation
Liver transplantation - UCSF criteria

141
Q

Criteria for liver transplant candidacy?

A

Uni of California, San Fran (UCSF criteria).
Single tumour <6.5cm, max 3 tumours with none >4.5cm + cumulative tumour size <8cm

142
Q

Palliative treament for HCC?

A

Local - ablation
Regional - Transarterial chemo-embolization (TACE), selective internal radiotherapy (Y-90)
Systemic - Sorafenib / Lenvatinib

143
Q

3 types of palliative therapy for HCC? (only 1st line for each)

A

Local - Radiofrequency ablation

Regional - Trans-arterial chemoembolization (TACE)

Systemic - Limited results - Sorafenib

144
Q

Commonest cause of secondary liver malignancy?

A

Colorectal CA

145
Q

Why is secondary liver malignancy more common than primary liver tumours? (10%)

A

Due to dual blood supply of liver.

146
Q

HX of Mets to liver parenchyma?

A

Fullness in RUQ, RHC pain.
Constitutional symptoms

147
Q

Hx of mets to porta-hepatis LNs?

A

Obstructive Jaundice

148
Q

PE of mets to liver parenchyma shows?

A

Hard, irregular, nodular hepatomegaly
Jaundice is late sign.

149
Q

PE of mets to porta-hepatis LNs shows?

A

Jaundice presents early and is progressive.
Hepatomegaly may not be present.

150
Q

Investigations of secondary liver CA in parenchyma?

A

LFT shows both obstructive and deranged liver enzymes.

151
Q

Investigations for mets to porta-hepatis LNs?

A

LFT shows obstructive jaundice

152
Q

Hepatic adenomas a/w?

A

Estrogen, anabolic steroids, progesterone prod, OCP

153
Q

Pyogenic hepatic abscess presents with?

A

RHC pain due to capsular stretch.
Diabetics x10 risk.

154
Q

Mirizzi’s syndrome?

A

CHD blockage secondary to extrinsic compression from an impacted gallstone in cystic duct or infundibulum of GB.

155
Q

Mirrizi’s syndrome a/w?

A

GB CA

156
Q

What is choledochal cyst?

A

Congenital cystic dilatation of extrahepatic and/or intrahepatic biliary tree

157
Q

How does DKA develop?

A

When body lacks insulin to allow blood sugar into cells for use as energy.
Instead, liver breaks down fat for fuel, a process that produces ketones. When too many ketones are produced too fast, DKA!

158
Q

5 routes of infections for pyogenic liver abscess?

A

Biliary tree 60%
Portal vein
Direct trauma
Hepatic artery
Adjacent organ infection

159
Q

Klatskin tumour arises where?

A

Bifurcation of intrahepatic ducts

160
Q

Options for drainage of hepatic abscess?

A

US-guided perQ drainage
Open drainage -> GS
Laparoscopic Drainage

161
Q

What is Caroli Disease?

A

Rare inherited disorder causing dilatation of large, intrahepatic BDs that appear as cysts on imaging and histopathologic exam.
Gene involved is same as AR PKD.

162
Q

what is Boerhaave syndrome?

A

Spontaneous perforation of 식도 due to rise in intraesophageal pressure.
E.g. severe straining or vomiting

163
Q

Hartmann’s pouch?

A

Diverticulum occurring at neck of GB

164
Q

What can loss of axillary hair mean?

A

Hyperestrogenism in CLD

165
Q

Caput medusae vs IVC obstruction causing venous dilatation in umbilical region?

A

Caput medusae shows blood going to LL
IVC blockage shows blood going up

166
Q

AST released from which cell part?

A

Mitochondria. Hence toxic stuff cause AST to fly

167
Q

ALT released from which cell part?

A

Cytosol. Hence viral infection cause ALT to fly

168
Q

How to differentiate Pyogenic vs Amoebic liver abscess on imaging?

A

Pyogenic liver abscess shows rim enhancement

169
Q

Investigations for amoebic liver abscess?

A

US/CTAP to confirm liver abscess.
Serum Ab testing to confirm organism

170
Q

How to evaluate pancreatic cyst?

A

1st line is MRI + MRCP

171
Q

Bouveret syndrome?

A

Form of gallstone-ileus caused by large GS that reach duodenal bulb and get lodged there

172
Q

Diagnose young pt with asymptomatic/periodic jaundice triggered by stress?

A

Gilbert’s syndrome

173
Q

LFT in HCC is not to confirm diagnosis but for staging?

A

Yes!

174
Q

How does chronic pancreatitis cause jaundice?

A

Jaundice in pancreatitis is usu due to hepatocellular injury or to associated biliary tract disease.
E.g., blockage of common bile duct due to pancreatic fibrosis, edema or pseudocyst.

175
Q

Complications of chronic pancreatitis?

A

Pseudocyst
Pancreatic ductal stones
Pancreatic ascites
Fistula
Pancreatic insufficiency - T1DM, steatorrhea, malnutrition, Vit deficiency
Duodenal / CBD obstruction

176
Q

Presentation of focal nodular hyperplasia?

A

Asymptomatic. OR
RUQ pain.

FNH rarely ruptures or bleeds

177
Q

Focal nodular hyperplasia on triphasic CT?

A

Bright homogenous arterial contrast enhancement with hypoattenuating central scar

178
Q

Focal nodular hyperplasia treatment options?

A

Conservative if asymptomatic.
Surgery if symptomatic

GS Medbear (14 decks)

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