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
1st line to investigate liver haemangioma?
US 1st choice. Accuracy 70-80%. Well-circumscribed, homogenous, hyperechoic lesion. ## Footnote Dont biopsy cuz risk of huge haemorrhage
26
How does liver haemangioma show on CT?
Triphasic CT Peripheral enhancement in arterial phase, centripetal filling on portal venous phase. Retention of contrast on delayed phase.
27
How to treat liver haemangioma?
Mostly treated safety with observation. Surgical removal for symptomatic or complicated
28
Diagnosis of acute pancreatitis?
**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
29
What causes death in acute pancreatitis?
Early - due to organ failure Late - infected pancreatic necrosis with resultant sepsis and multi-organ failure
30
2 commonest causes of acute pancreatitis?
Gallstones and alcohol. 60-80% of casess
31
Pathophysiology of acute pancreatitis - auto digestion?
Unregulated activation of trypsin within pancreatic acinar cells. Pro-enzymes activated causing auto-digestion.
32
Pathophysiology of acute pancreatitis - gallstones?
Obstructed pancreatic duct causing higher pressure in pancreatic duct Extravasation of pancreatic juice leading to injury of gland.
33
Pathophysiology of acute pancreatitis - interstitial edema due to gallstone blockage?
Impaired blood flow to cells causing ischaemic cellular injury. Proenzymes activated causing pancreatic acinar cell damage.
34
Which body posture alleviates acute pancreatitis pain?
Sitting up and leaning forward
35
Normal serum amylase level?
30-100U/L Levels rise within a few hrs but normalize in 5 days Elevation for >10 days indicate complications like pseudocysts ## Footnote Can miss later presentations of pancreatitis
36
Normal Serum lipase level?
10-140 U/L Levels rise within 4-8 hrs and stay elevated for 8-14 days
37
How to use C-Reactive Protein levels?
Risk stratification for acute pancreatitis. >150mg/L within 48 hrs a/w severe pancreatitis
38
Where is CEA elevated?
Most adenoCAs. CRC, pancreatic, breast, lung, gastric, cholangio, endometrial, medullary thyroid Others: IBD, Pancreatitis, Hepatitis
39
Early local complication of acute pancreatitis?
Acute peripancreatic fluid collection - Due to increased vascular permeability. Acute necrotic collection - 30% develop secondary bacterial infection - Enteric GNR
40
How to tell if acute necrotic collection is sterile or infected?
Infected if have gas bubbles on CT / persistent sepsis / progressive clinical deterioration. Positive culture can be obtained from FNA or during drainage procedure
41
Late local complication of acute pancreatitis? > 4 weeks
Pancreatic pseudocyst. Presents as persistent pain, mass on exam, persistent high amylase or lipase
42
3 signs of haemorrhagic pancreatitis?
Grey-turner sign - flank ecchymosis Cullen's sign - periumbilical ecchymosis Fox's sign - inguinal ecchymosis
43
Complications of pseudocyst
Fistula formation Hemorrhage Rupture - pancreatic ascites Obstruction - intestinal, vascular, biliary, gastric outlet Infection - abscess
44
Are serum amylase and lipase useful in chronic pancreatitis?
No. Commonly normal cuz significant fibrosis causing lower abundance of these enzymes within pancreas.
45
Whipple procedure?
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.
46
Commonest pancreatic CA?
Ductal adenoCA. Others include adenosquamous CA, SCC, Acinar cell CA.
47
Presentation of pancreatic CA?
Vague epigastric discomfort and presence of constitutional symptoms despite normal upper endoscopy should prompt further investigations.
48
Symptoms and signs of pancreatic CA?
Classical Courvoisier sign Obstructive jaundice with pain New onset DM in elderly patients Signs of malabsorption N/V LOW, anorexia Upper BGIT
49
Signs of advanced malignancy in pancreatic CA?
Malignant pleural effusion Virchow's Node Trousseau sign of malignancy Sister Mary Joseph Nodule Hepatomegaly Nonbacterial thrombotic endocarditis ## Footnote Must differentiate Trousseau from in hypoCa
50
Important test for Pancreatic CA?
Carbohydrate Antigen 19-9 (CA19-9) Can act as prognostic marker - lower the better. Poor sensitivity and specificity.
51
CA19-9 elevated in which pathos?
Lung CA, Gastric CA, CRC, biliary tract CA, urothelial CA Pancreatitis, hepatitis, thyroiditis, biliary obstruction
52
What can be seen in transabdominal US in pancreas stuff?
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
53
Commonest staging modality for pancreatic CA?
Tri-phasic "Pancreatic protocol CT scan" and CT thorax
54
What is double duct sign in CT for pancreatic CA?
Simultaneous dilatation of CBD (intra-pancreatic segment) and pancreatic duct
55
Reason for ERCP stenting post-op in acute pancreatic CA?
Relieve biliary obstruction. BUT raise risk of post-op complications in patients with resectable disease
56
Pylorus-preserving Pancreatico-duodenectomy Resection - PPPDR?
Preserve gastric antrum, pylorus, proximal DDM - DDM transected at least 2cm distal to pylorus.
57
Signs of chronic liver disease on PE?
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
58
Courvoisier's law?
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
59
Commonest causes of obstructive jaundice?
Gallstones Tumour Hepatitis
60
Painful obstructive jaundice causes
Gallstones, strictures, hepatic causes
61
Painless obstructive jaundice causes
Periampullary tumour
62
What is periampullary tumour?
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
63
Pain comes in which stage of pancreatic CA? Consistency of pain?
Pain is a late symptom of pancreatic CA. Constant and relentless compared to biliary colic which subsides after a few hours.
64
Pain comes in which stage of pancreatic CA? Consistency of pain?
Pain is a late symptom of pancreatic CA. Constant and relentless compared to biliary colic which subsides after a few hours.
65
Relevant Hx for pancreatic head CA?
New onset DM/Recalcitrant CA. Dull aching pain radiating to back Pseudo Gastric outlet obstruction - duodenal obstruction *Worsening steatorrhea*
66
AST / ALT ratio of >2:1 indicates?
Alcoholic liver disease
67
Management option for jaundice?
ERCP - use of upper endoscopy and fluoroscopy to evaluate biliary system.
68
Therapeutic use of ERCP?
Removal of common duct stones with sphincterotomy and/or relief of biliary obstruction with biliary stent.
69
Diagnostic use of ERCP?
Brushing, biopsy, FNAC for malignancy
70
Types of gallstones?
Cholesterol stone 85% Pigment stones 15%
71
5Fs in cholesterol gallstones
Fertility Female Fat Forty Family hx
72
Difference between cholesterol and pigment stones
Black, sterile, hard, Radiolucent = Cholesterol stone Brown, infected, soft, Radio-opaque = Pigment stones
73
What posture must u ask pt to do if u see abdominal scar?
Tilt head forward. This will reveal incisional hernia.
74
Where does gallstone pain radiate to?
Inferior angle of scapula or tip of right shoulder
75
Timing of gallstone pain?
Distinct attacks lasting 30 mins to several hours. Often resolve by 6hrs. If not then suspect complications.
76
What is decompensated cirrhosis?
Development of ascites, HE, GI Bleeding. Poor survival rate unless transplant.
77
How to classify COMPLICATED CHOLELITHIASIS?
By organ! In GB, Common BD, in Gut
78
Complicated gallstone in GB?
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
Complicated gallstone in common bile duct?
Choledocholithiasis - causing: - Obstructive jaundice - Ascending cholangitis - Secondary biliary cirrhosis - Gallstone pancreatitis.
80
Indications for gallstone surgery?
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
What % of patients still have abdo pain post-cholecystectomy?
10-41%
82
What technique for Lap Cholecystectomy?
Hasson Open Technique. 3x 5mm ports inserted in subxiphoid, right subcostal area and right flank.
83
How does gallstone or biliary sludge cause acute cholecystitis?
Block cystic duct -> high intraluminal pressure within GB -> compromise blood flow and lymphatic drainage within GB wall. Mucosal ischemia and necrosis results.
84
Are cultures from GB in cholecystitis sterile?
Initially sterile, but eventually secondary bacterial infection with enteric organism can occur.
85
History of acute calculous Cholecystitis?
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
What signs in abdomen can be seen in acute calculous cholecystitis?
RHC tenderness with guarding Murphy's sign Palpable GB (30%)
87
Radiological findings of calculous cholecystitis?
US HBS 1st line. Thickened GB wall with edema. Contracted GB.
88
What is elevated in acute cholecystitis blood test?
TW>18 means need to consider complications. High CRP - consider complicated Gallstone disease High ALP in LFT. U/E/Cr - dehydration. High amylase
89
Empirical IV Abx for acute calculous cholecystitis?
Ceftriaxone and metronidazole.
90
Common organisms for infection in acute calculous cholecystitis?
E. Coli Klebsiella Pseudomonas Enterococcus
91
Conservative management for calculous cholecystitis?
Monitor vitals and resuscitate if needed Septic workup Analgesia Empirical IV Abx
92
Lap cholecystectomy options?
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
Immediate treatment for acute calculous cholecystectony?
Percutaneous cholecystectomy for those not fit for surgery. E.g. early surg hard due to extensive inflamm or gangrenous GB with thin wall
94
Complications of cholecystectomy?
Hydrops Empyema Cholecystoenteric fistula Gangrene and perforation Emphysematous cholecystitis Gallstone ileus
95
Primary pathology of acute Acalculous cholecystitis?
GB distension with bile stasis and ischemia
96
Risk factors for acalculous cholecystitis?
Prolonged ICU stay Sepsis with hypotension Extensive burns / multiple trauma Patients on total PO nutrition - cause biliary stasis
97
Clinical presentation of acalculous cholecystitis?
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
What proportion of cholecystectomy patients have choledocholithiasis?
5-20% at time of surgery
99
Biochemical markers for CBD gallstones?
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
PE of CBD gallstones?
Septic looking, jaundice Vitals - febrile, hypotension Abdomen - RUQ/epigastric tenderness Palpable GB.
101
2 approaches to gallstones in CBD?
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
What is Mirizzi's syndrome?
Common hepatic duct obstruction secondary to extrinsic compression from an impacted gallstone in cystic duct or infundibulum of GB
103
Charcot's TRIAD OF CHOLANGITIS?
FEVER JAUNDICE RUQ PAIN
104
HOW DO BACTERIA ENTER BILE AND BILIARY TRACT IN CHOLANGITIS?
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
Additional 2 criteria for Reynold's Triad in Cholangitis?
Hypotension Altered mental state
106
Management goals of cholangitis?
Treat biliary infection and obstruction Resuscitate if have septic shock. Consider Emergent biliary decompression with ERCP.
107
What empirical Abx for cholangitis?
IV Ceftriaxone and metronidazole. Imipenem if patient is in shock
108
Risk factors for GB CA?
Cholelithiasis. Larger and symptomatic stones a/w higher risk Calcified GB GB polyps Others
109
Clinical presentation of GB CA?
Asymptomatic - incidental histological finding after cholecystectomy. Early - mimic gallstone inflamm Late - biliary and stomach obstruction
110
US signs for GB CA?
US - thickened irregular GB wall or mass replacing GB with invasion of liver. Doppler signal in GB mass. Enlarged LNs Dilated biliary tree
111
CTAP uses for GB CA?
Needed for staging, assessment of local invasion but poor for nodal spread. Hence do prior to definitive surgery.
112
MRCP uses for GB CA?
Allows complete assessment of biliary, vascular, nodal, hepatic and adjacent organ involvement
113
1 stage vs 2 stage cholecystectomy for GB CA?
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
Commonest cholangioCA?
AdenoCA
115
Risk factors for cholangioCA?
Chronic cholestasis - causing prolonged inflamm of biliary epithelium. Congenital biliary tract disorders DM
116
Clinical Presentation of cholangioCA?
Intrahepatic - non specific symptoms Extrahepatic - painless progressive obstructive jaundice Dark urine, pale stools, pruritus LOW/LOA Malaise, fatigue, night sweats
117
PE of cholangioCA?
Jaundice (90%) Hepatomegaly (25-40%) RUQ mass (10%) Fever (2-14%) RUQ tenderness
118
Classification of cholangioCA?
A few ways. Anatomical location - INTRAHEPATIC (5-10%) vs HILAR (60-70%) vs EXTRAHEPATIC (20-30%)
119
Classification for hilar lesions in cholangioCA?
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
Biochemical tests for cholangioCA?
FBC/RP/PT, INR, APTT LFT - non specific rise in serum BRB, high ALP + GGT High C19-9 High CEA
121
US findings for cholangioCA? (first line)
US HBS - first line. Check biliary duct dilatation. Can localize site of obstruction
122
Imaging options for cholangioCA?
US HBS CT triphasic Cholangiography (MRCP / ERCP) Endoscopic US with FNA PET-CT
123
Prognosis of cholangioCA?
Most patients have unresectable disease at presentation and die within a year. 5 year survival rates post surgeries is like 50% max.
124
Management option for cholangioCA?
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
Criteria for unresectability of hilar lesions?
Vascular involvement Extent of distant spread Extent of local disease
126
Management options for pancreatic CA?
Chemo and Radiotherapy. Surgery with curative resection.
127
When is HCC mostly diagnosed?
In 5th and 6th decade
128
Risk factors for HCC?
CLD, HBV/HCV infection, cirrhosis (alcoholic and non-alcoholic)
129
Molecular classification for HCC?
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
Histological subtypes of HCC?
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
Gold standard for HCC imaging?
Triphasic CT Scan
132
What to investigate for in HCC after confirming HCC?
Stage disease, mainly with CT scan and assess tumour burden Assess liver function Check for complications of disease and for pre-operative assessment.
133
Radiological hallmark between HCC and haemangioma?
HCC mets shows portal venous enhancement Haemangioma shows capsular enhancement in delayed phase.
134
Which vessel does HCC invade most commonly?
Portal vein. Can show enhancing portal vein thrombus.
135
How to assess liver function for staging of HCC?
Biochemical tests -> Child-Pugh score Indocyanine green assessment (ICG) CT volumetry/MR volumetry
136
Child-Pugh Score?
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
How to use ICG assessment for HCC? | Indocyanine green
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
What is CT volumetry / MR volumetry used for in HCC?
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
How to assess patient's performance status in HCC?
ECOG performance scale 4 means ADL dependent and totally confined to bed/ chair
140
Curative treatment modality for HCC management?
Curative: surgical resection +- ablation Liver transplantation - UCSF criteria
141
Criteria for liver transplant candidacy?
Uni of California, San Fran (UCSF criteria). Single tumour <6.5cm, max 3 tumours with none >4.5cm + cumulative tumour size <8cm
142
Palliative treament for HCC?
Local - ablation Regional - Transarterial chemo-embolization (TACE), selective internal radiotherapy (Y-90) Systemic - Sorafenib / Lenvatinib
143
3 types of palliative therapy for HCC? (only 1st line for each)
Local - Radiofrequency ablation Regional - Trans-arterial chemoembolization (TACE) Systemic - Limited results - Sorafenib
144
Commonest cause of secondary liver malignancy?
Colorectal CA
145
Why is secondary liver malignancy more common than primary liver tumours? (10%)
Due to dual blood supply of liver.
146
HX of Mets to liver parenchyma?
Fullness in RUQ, RHC pain. Constitutional symptoms
147
Hx of mets to porta-hepatis LNs?
Obstructive Jaundice
148
PE of mets to liver parenchyma shows?
Hard, irregular, nodular hepatomegaly Jaundice is late sign.
149
PE of mets to porta-hepatis LNs shows?
Jaundice presents early and is progressive. Hepatomegaly may not be present.
150
Investigations of secondary liver CA in parenchyma?
LFT shows both obstructive and deranged liver enzymes.
151
Investigations for mets to porta-hepatis LNs?
LFT shows obstructive jaundice
152
Hepatic adenomas a/w?
Estrogen, anabolic steroids, progesterone prod, OCP
153
Pyogenic hepatic abscess presents with?
RHC pain due to capsular stretch. Diabetics x10 risk.
154
Mirizzi's syndrome?
CHD blockage secondary to extrinsic compression from an impacted gallstone in cystic duct or infundibulum of GB.
155
Mirrizi's syndrome a/w?
GB CA
156
What is choledochal cyst?
Congenital cystic dilatation of extrahepatic and/or intrahepatic biliary tree
157
How does DKA develop?
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
5 routes of infections for pyogenic liver abscess?
Biliary tree 60% Portal vein Direct trauma Hepatic artery Adjacent organ infection
159
Klatskin tumour arises where?
Bifurcation of intrahepatic ducts
160
Options for drainage of hepatic abscess?
US-guided perQ drainage Open drainage -> GS Laparoscopic Drainage
161
What is Caroli Disease?
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
what is Boerhaave syndrome?
Spontaneous perforation of 식도 due to rise in intraesophageal pressure. E.g. severe straining or vomiting
163
Hartmann's pouch?
Diverticulum occurring at neck of GB
164
What can loss of axillary hair mean?
Hyperestrogenism in CLD
165
Caput medusae vs IVC obstruction causing venous dilatation in umbilical region?
Caput medusae shows blood going to LL IVC blockage shows blood going up
166
AST released from which cell part?
Mitochondria. Hence toxic stuff cause AST to fly
167
ALT released from which cell part?
Cytosol. Hence viral infection cause ALT to fly
168
How to differentiate Pyogenic vs Amoebic liver abscess on imaging?
Pyogenic liver abscess shows rim enhancement
169
Investigations for amoebic liver abscess?
US/CTAP to confirm liver abscess. Serum Ab testing to confirm organism
170
How to evaluate pancreatic cyst?
1st line is MRI + MRCP
171
Bouveret syndrome?
Form of gallstone-ileus caused by large GS that reach duodenal bulb and get lodged there
172
Diagnose young pt with asymptomatic/periodic jaundice triggered by stress?
Gilbert's syndrome
173
LFT in HCC is not to confirm diagnosis but for staging?
Yes!
174
How does chronic pancreatitis cause jaundice?
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.
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Complications of chronic pancreatitis?
Pseudocyst Pancreatic ductal stones Pancreatic ascites Fistula Pancreatic insufficiency - T1DM, steatorrhea, malnutrition, Vit deficiency Duodenal / CBD obstruction
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Presentation of focal nodular hyperplasia?
Asymptomatic. OR RUQ pain. | FNH rarely ruptures or bleeds
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Focal nodular hyperplasia on triphasic CT?
Bright homogenous arterial contrast enhancement with hypoattenuating central scar
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Focal nodular hyperplasia treatment options?
Conservative if asymptomatic. Surgery if symptomatic