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Surgery > Hepatobiliary > Flashcards

Hepatobiliary Flashcards

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
Q

Management of hepatic encephalopathy

A

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
Q

Investigations in HCC

A

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
Q

Staging of HCC

A

Based on tumour number and extent
Child-Pugh score
AFP level
Portal vein thrombosis

28
Q

Management options of HCC

A

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
Q

Stats regarding HCC site

A

75% portal vein invasion
75% bilobar
65% have 3 or more distinct tumours present

30
Q

Causes of HCC

A

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
Q

Average survival for HCC

A

6 months
Less than 5% 2 year survival if unresectable HCC
High recurrence regardless of treatment

32
Q

Definition of biliary colic

A

Pain associated with the temporary obstruction of the cystic or common bile duct by a stone migrating from the gall bladder

33
Q

Types of biliary stones

A

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
Q

Clinical features of biliary colic

A

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
Q

Management of biliary colic

A

Opiate analgesia
Stone extraction via ERCP
OR
Laparoscopic cholecystectomy with bile duct exploration
Cholecystectomy to prevent recurrence in surgical candidates

36
Q

Complications of biliary colic

A

Gallstone pancreatitis

Acute cholangitis

37
Q

Presentation of acute/ascending cholangitis

A

Charcot’s triad:

  • fever
  • jaundice
  • abdominal pain
38
Q

Management of acute cholangitis

A

Antibiotics (ampicillin or tazocin)

39
Q

Causes of acute cholecystitis

A 
Gallstones (95%)
Ischaemia in critically ill patient
Infection, especially in AIDs (CMV, cryptosporidium)
Bile duct strictures
Neoplasms
40
Q

What is Mirizzi syndroem

A

Mild jaundice in acute cholecystitis caused by external compression of the common bile duct by a stone within the gallbladder or cystic duct

41
Q

USS findings of cholecystitis

A

Shadowing of stones
Dilated gallbladder with thickened wall
Surrounding oedema

42
Q

Management of cholecystitis

A 
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
Q

Complications of acute cholecystitis

A

Empyema or gangrene
failure to respond to conservative management (especially if increased pain and fever)
URGENT IMAGING
Surgical intervention required

44
Q

Risk factors for acute pancreatitis

A

Gallbladder disease
Chronic alcohol consumption
Autoimmune disease (E.g. SLE)
Congenital anomalies

45
Q

Causes of acute pancreatitis

A 
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
Q

Investigations in acute pancreatitis

A

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
Q

grading severity of acute pancreatitis

A 
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
Q

Management of acute pancreatitis

A 
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
Q

Complications of chronic pancreatitis

A

Pancreatic pseudocyst
Ascites, pleural effusions
Pancreatic cancer

50
Q

Definition of pancreatic pseudocyst

A

Fluid collection in the pancreas surrounded by granulation tissue occurring in a period of enhanced inflammatory activity with abdominal pain

51
Q

Most common type of pancreatic cancer

A

Adenocarcinoma (96%)
mostly of ductal origin
Most commonly in the head of the pancreas

52
Q

Hereditary pancreatic cancer syndromes

A

BRCA2
Familial atypical multiple mole melanoma
Peutz-Jeghers syndrome
Hereditary pancreatitis

53
Q

What is Courvoisier’s law

A

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
Q

Presentation of carcinoma of head of pancreas or ampulla of vater

A

Painless
Jaundice
Scratch marks/pruritus
palpable gall bladder

thromboembolic phenomena
Polyarthritis
Skin nodules

55
Q

Complications of carcinoma of the head of the pancreas

A

Episodes of acute pancreatitis

Pancreatic damage - abnormal glucose homeostasis

56
Q

Presentation of carcinoma of the body or tail of the pancreas

A 
Abdominal pain (dull, radiating to back, partial relief by sitting forward)
Non-specific (anorexia, weight loss)

thromboembolic phenomena
Polyarthritis
Skin nodules

57
Q

investigations in pancreatic cancer

A

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
Q

Associated with CA19-9

A

Pancreatic cancer

59
Q

Which tumour marker is associated with pancreatic cancer

A

CA19-9

60
Q

Red flags of chronic diarrhoea/abdominal pain (i.e. not IBS)

A 
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
Q

Management of IBS

A

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)

Surgery (8 decks)

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