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Hepatobiliary Flashcards

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1
Q

Presentation of acute pancreatitis

A 
Abdominal pain (epigastric, radiation to back, persists for days, reaches max intensity over 30-60min then remains stable)
Nausea, vomiting

Tachycardia
Hypotension
Tachypnoea
Reduced saturations
Guarding of the abdomen

Cullen’s and Grey Turners sign may also be present

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2
Q

Cullen’s sign

A

Superficial oedema and bruising around the umbilicus

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3
Q

Grey Turner’s sign

A

Bruising on the flanks of the body

  • sign of retroperitoneal haemorrhage
  • takes 24-48 hours to develop
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4
Q

Causes of chronic liver disease

A

NASH
Alcoholic SH
Chronic viral hepatitis (hep B/C)
Autoimmune/ Cholestasis (primary biliary cirrhosis, primary sclerosing cholangitis)
Inherited metabolic disorders (haemochromatosis, Wilson’s disease

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5
Q

Hep B serology

A

HBsAg = active infection (acute or chronic)
Anti-HBs = Immunity (vaccination or cleared infection)
Anti-HBc - infection (past or current)

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6
Q

Management chronic Hep B

A

No cure
Reduce risk of other liver diseases
Entecavir or tenofovir

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7
Q

Hepatitis C serology

A

Anti-HCV antibody

HCV RNA qualitative PCR

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8
Q

Management of chronic hep C

A

Genotype 1: telaprevir/boceprevir + Peg-IFNa + ribavirin

Other genotypes: Peg-IFNa + ribavirin

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9
Q

Management of primary biliary cirrhosis

A

Ursodeoxycholic acid/UDCA (reduces gallstones)

Liver transplant if severe

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10
Q

Diagnosis of primary biliary cirrhosis

A

Raised ALP and bilirubin
Antimicrobial antibodies
ANA
Liver biopsy (lymphocytic invasion of ducts)

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11
Q

Diagnosis of primary sclerosing cholangitis

A

Cholestatic picture in LFTs
+ve pANCA
MRCP/ERCP - multifocal stricturing

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12
Q

Management of primary sclerosing cholangitis

A

High dose UDCA (ursodeoxycholic acid)
Endoscopic dilatation of dominant structures
Liver transplantation
Symptom relief

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13
Q

Cirrhosis staging

A 
Child-Pugh score:
Total bilirubin (34-50)
Serum albumin (3.5-2.8)
PT INR (1.7-2.3)
Ascites
Hepatic encephalopathy
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14
Q

Child pugh score and prognosis

A 
5-6 = A 100%1y, 85% 2y
7-9 = B 80% 1y, 60% 2y
10-15 = C 45% 1y, 35% 2y
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15
Q

Complications of cirrhosis

A 
Ascites
Oesophageal/gastric varices
Spontaneous bacterial peritonitis
Hepatic encephalopathy
Pulmonary syndromes
Hepatocellular cancer
Hepatorenal syndrome
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16
Q

Ascitic tap fluid

A

Serum ascites-to-albumin gradient (SAAG)
- over 11g/L - portal hypertension cause of ascites
- Less than 11g/L - consider infectious or malignant cause
Blood cell count:
- High RBCs - traumatic tap? HCC? Ruptured omental varix?
- High PMNs - infection
Culture
+/- amylase or cytology

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17
Q

Management of ascites

A

Small:
- dietary sodium restrictions (6-8g/day)
Moderate:
- diuretic therapy (spironolactone +/- frusemide)
Refractory:
- repeated large-volume paracentesis
- transjugular intrahepatic portosystemic shunt

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18
Q

What is hepatic hydrothorax?

A

Flow of ascitic fluid into the thoracix cavity due to a tear in the diaphragm
More common on the right side

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19
Q

Prognosis following onset of ascites in chronic liver disease

A

Poor. Less than 50% will survive 2y after onset of ascites

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20
Q

Definition of spontaneous bacterial peritonitis

A

A common and severe complications of ascites characterised by spontaneous infection of the ascitic fluid without an intraabdominal source

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21
Q

Most common organisms implicated in spontaneous bacterial peritonitis

A 
E. coli
Other gut bacteria
S. viridans
S. aureus
Enterococcus

If more than 2 organisms identified ?perforated viscus

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22
Q

Management of spontaenous bacterial peritonitis

A

Cefotaxime or another 2nd generation cephalosporin

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23
Q

Definition of hepatic encephalopathy

A

AKA portosystemic encephalopathy, an alteration in mental status and cognitive function in the presence of liver failure due to vascular shunting allowing nitrogenous metabolites to bypass hepatic filtration, thus reaching the brain and causing damage to neurons

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24
Q

Clinical features of hepatic encephalopathy

A

Confusion
Change in personality (violent, difficult to manage)
Sleepy, difficult to rouse
Asterixis/hepatic flap

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25
Management of hepatic encephalopathy
management of precipitating factors (hydration and correction of electrolytes may be all the treatment required) Lactulose (elimination of nitrogenous products in the gut via cathartis)
26
Investigations in HCC
Alpha fetoprotein (only increased in 50%) AFP-L3 is more specific Imaging: USS liver, triphasic CT abdo/pelvis Core liver biopsy - allows distinction between HCC and adenocarcinoma - higher bleeding risk compared to other cancers
27
Staging of HCC
Based on tumour number and extent Child-Pugh score AFP level Portal vein thrombosis
28
Management options of HCC
Presence of cirrhosis usually restricts surgical resection, ablative therapies and CTx Resection Transplant Local injection therapy (ethanol - max tumour size 3cm) TACE (transcatheter arterial chemoembolisation) New agents (sorafenib, bevacizumab + erlotinib) Radiation therapy (if less than 2cm)
29
Stats regarding HCC site
75% portal vein invasion 75% bilobar 65% have 3 or more distinct tumours present
30
Causes of HCC
Hepatitis - Chronic HBV (only 50% have cirrhossi) - Chronic HCV (only after cirrhosis) Cirrhosis of any cause (less so for PBC or haemochromatosis) Alfatoxin B1 (product of aspergillus) found in stored grains/rice/peanuts in humid conditions
31
Average survival for HCC
6 months Less than 5% 2 year survival if unresectable HCC High recurrence regardless of treatment
32
Definition of biliary colic
Pain associated with the temporary obstruction of the cystic or common bile duct by a stone migrating from the gall bladder
33
Types of biliary stones
Black pigment gallstones: - calcium bilirubinate + mucin glycoproteins + salts e.g. calcium carbonate - range in colour from deep black to very dark brown - glass-like cross-sectional surface on fracturing Brown stones: - muddy hue - alternating brown/tan layers on cross-section - calcium salts of fatty acids + calcium bilirubinate - almost always found in presence of stasis and/or infection - most common cause of recurrent bile duct stones following cholecystectomy
34
Clinical features of biliary colic
Abdominal pain: - epigastric - radiation to R shoulder tip - severe - constant with cresecendo characteristic - often following over indulgence with food (esp. high fat content) Nausea/vomiting Spontaneous cessation of attack after a number of hours or terminated by opiate analgesia more protracted pain, esp with fevers and rigors, suggests secondary complications such as cholecystitis, cholangitis or gallstone-related pancreatitis
35
Management of biliary colic
Opiate analgesia Stone extraction via ERCP OR Laparoscopic cholecystectomy with bile duct exploration Cholecystectomy to prevent recurrence in surgical candidates
36
Complications of biliary colic
Gallstone pancreatitis | Acute cholangitis
37
Presentation of acute/ascending cholangitis
Charcot's triad: - fever - jaundice - abdominal pain
38
Management of acute cholangitis
Antibiotics (ampicillin or tazocin)
39
Causes of acute cholecystitis
``` Gallstones (95%) Ischaemia in critically ill patient Infection, especially in AIDs (CMV, cryptosporidium) Bile duct strictures Neoplasms ```
40
What is Mirizzi syndroem
Mild jaundice in acute cholecystitis caused by external compression of the common bile duct by a stone within the gallbladder or cystic duct
41
USS findings of cholecystitis
Shadowing of stones Dilated gallbladder with thickened wall Surrounding oedema
42
Management of cholecystitis
``` nil by mouth IV fluids Opiate analgesia IV antibiotics (local policy) - extended-spectrum cephalosporins - fluoroquinolones - tazocin ``` Cholecystectomy delayed for a few days to allow symptoms and inflammation to settle
43
Complications of acute cholecystitis
Empyema or gangrene failure to respond to conservative management (especially if increased pain and fever) URGENT IMAGING Surgical intervention required
44
Risk factors for acute pancreatitis
Gallbladder disease Chronic alcohol consumption Autoimmune disease (E.g. SLE) Congenital anomalies
45
Causes of acute pancreatitis
``` Gallstones (70-80%) Chronic alcohol binges Other drugs/toxins Metabolic (hyperlipidaemia, hypercalcaemia) Trauma (most commonly post-ERCP) Non-gallstone obstruction of pancreatic duct (stricture, neoplasm, sphincter of Oddi dysfunction) Infections (CMV, mumps, rubella) Genetics (CF) Autoimmune Idiopathic ```
46
Investigations in acute pancreatitis
Amylase and lipase- 3x upper limit of normal Blood urea nitrogen CBE (raised haematocrit and WCC) Liver enzymes (ALT ?gallstones) CT abdo - pancreatic necrosis best seen approx 3 days after presentation MRCP if gallstones suspected
47
grading severity of acute pancreatitis
``` APACHE II Takes into account 12 continuous variables 1. body temp 2. mean arterial pressure 3. heart rate 4. respiratory rate 5. oxygenation 6. sodium 7. potassium 8. phosphate 9. creatinine 10. haematocrit 11. WCC 12. GCS ```
48
Management of acute pancreatitis
``` General supportive care - Nil by mouth until bowel sounds and appetite return - Parenteral opioids - IV fluid repletion - anti-emetics (IV promethazine) Treatment of complications ```
49
Complications of chronic pancreatitis
Pancreatic pseudocyst Ascites, pleural effusions Pancreatic cancer
50
Definition of pancreatic pseudocyst
Fluid collection in the pancreas surrounded by granulation tissue occurring in a period of enhanced inflammatory activity with abdominal pain
51
Most common type of pancreatic cancer
Adenocarcinoma (96%) mostly of ductal origin Most commonly in the head of the pancreas
52
Hereditary pancreatic cancer syndromes
BRCA2 Familial atypical multiple mole melanoma Peutz-Jeghers syndrome Hereditary pancreatitis
53
What is Courvoisier's law
In the presence of an enlarged, non-tender gallbladder + mild jaundice, the diagnosis is unlikely to be gallstones and more likely to be malignancy of the head of the pancreas
54
Presentation of carcinoma of head of pancreas or ampulla of vater
Painless Jaundice Scratch marks/pruritus palpable gall bladder thromboembolic phenomena Polyarthritis Skin nodules
55
Complications of carcinoma of the head of the pancreas
Episodes of acute pancreatitis | Pancreatic damage - abnormal glucose homeostasis
56
Presentation of carcinoma of the body or tail of the pancreas
``` Abdominal pain (dull, radiating to back, partial relief by sitting forward) Non-specific (anorexia, weight loss) ``` thromboembolic phenomena Polyarthritis Skin nodules
57
investigations in pancreatic cancer
Transabdominal ultrasound - less reliable in picking up tumours in body and tail due to overlying bowel Contrast CT Laparoscopy ERCP (restricted to palliative treatment usually, provide source of cytology if unclear) Percutaneous needle biopsy (discouraged in operable cases, essential prior to palliative chemotherapy) Tumour marker CA19-9
58
Associated with CA19-9
Pancreatic cancer
59
Which tumour marker is associated with pancreatic cancer
CA19-9
60
Red flags of chronic diarrhoea/abdominal pain (i.e. not IBS)
``` Weight loss Rectal bleeding Onset after 55y Nocturnal pain Family history of malignancy or IBD Abnormal examination (mass, enlarged LN, muscle wasting, +ve FOBT etc.) Abnormal laboratory investigations ```
61
Management of IBS
Low FODMAP diet High-fibre intake Avoid aggravating foods, caffeine, dairy, fatty foods CBT (if psychosocial stressors are important triggers) Regular exercise, adequate fluid intake Sedatives of SSRIs (esp in patients who appear anxious)

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