The Surgical Review- Hepatobiliary and Pancreas Flashcards

1
Q

What are the five different types of choledochal cysts?

A

I: Fusiform: dilation of CBD
II: isolated diverticulum protruding from the CBD
III: dilation of duodenal portion of CBD
IV: multiple dilations of intra and extra hepatic biliary tree
V (Caroli disease): intrahepatic without extra hepatic

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2
Q

What is the treatment of type I, II and V?

A

I and II: Roux en y

V: liver txp

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3
Q

patients with Primary sclerosing cholangitis have an increased risk for development of what type of cancer?

A

cholangiocarcinoma (follow them with serial CA19-9)

PSC assoc w UC

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4
Q

what test is the most sensitive and specific for the diagnosis of pyogenic liver abscess?

A

CT

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5
Q

Which bugs usually cause pyogenic liver abscess?

A

polymicrobial consisting of:

  • klebsiella
  • e coli
  • streptococci
  • bacteroides fragilis
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6
Q

Treatment of pyogenic liver abscess?

A

IR percutaneous drainage _ broad spectrum antibiotics

open surgical drainage is reserved for septic patients who fail percutaneous drainage

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7
Q

Which AMEBA causes liver abscesses and which populations do they affect?

A
  • Entamoeba histolytica
  • infects alcoholic and homosexual pts
  • ingested then migrate from intestine to liver
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8
Q

Treatment entamoeba histolytic abscess?

A

14 days metronidazole

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9
Q

what bug cases hydatid liver disease (cysts)?

A

Echinococcus granulosum (tapeworm)

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10
Q

treatment of hydatid cyst?

A

surgical resection is definitive, only 50% respond to albendazole
- cysts are highly antigenic and rupture may result in anaphylactic shock

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11
Q

who are the definitive hosts for echinococcus granulosum?

A

dogs!
but humans get it after ingesting the eggs from sheep or cattle
- eggs penetrate the small bowel and migrate via the portal blood system

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12
Q

2 causes of bleeding gastric varices?

A
  1. Portal HTN 2/2 cirrhosis (TIPS)

2. Splenic vein thrombosis (perform splenectomy)

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13
Q

why do gastric varies provide a greater therapeutic challenge than esophageal varices?

A

their deeper submucosal position may preclude effective endoscopic therapy

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14
Q

What are the contraindications to TIPS?

A
  1. Right sided heart failure with increased CVP
  2. Severe hepatic failure
  3. Portal vein thrombosis
  4. Severe hepatic encephalopathy
  5. Active local or systemic infection
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15
Q

treatment of bleeding gastroesophageal varices?

A

endoscopic band ligation + serial endoscopy with banding

tips is second tier option

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16
Q

What are the different types of portosystemic shunts?

A
  1. Nonselective shunts: portocaval or mesocaval, decompress the entire portal system
  2. Selective: distal splenorenal (warren), decompress the gastroesophageal bed only thus decreased risk of hepatic failure
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17
Q

what is the Child’s Pugh score and what factors does it take into account? 5 factors

A
  • score that classifies liver failure
    1. Serum bilirubin
    2. Serum albumin
    3. Ascites
    4. Encephalopathy
    5. Nutrition
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18
Q

What is the MELD score and what factors does it use?

A

Model for End Stage Liver Disease: pre and post surgical mortality associated with cirrhosis

  1. Creatinine
  2. Bilirubin
  3. INR
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19
Q

Formula for MELD? teehee

A

= 0.957xlog(Cr)
+ 0.378xlog(Bilirubin)
+ 1.120xlog(INR)

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20
Q

What are the most common benign solid tumors of the liver?

A

Hemangiomas: rarely bleed or cause symptoms, only when >10cm

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21
Q

treatment of hemangiomas?

A

observe!

unless huge and symptomatic and surgical tx is warranted: enucleation

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22
Q

what is Kasabach-Merritt syndrome?

A

Hemangioma + thrombocytopenia and consumptive coagulopathy

  • thus surgical enucleation of hemangioma
  • mostly seen in kids, assoc w high mortality
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23
Q

management of benign hepatic cysts?

A

observe

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24
Q

how do you distinguish between Focal Nodular Hyperplasia and hepatic adenoma?

A

MRI can distinguish lesions

- confirmatory study: technetium-99m sulfur colloid scan, the Kupffer cells of FNH will take up radionuclide

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25
Q

what is Focal nodular Hyperplasia?

A
  • hyperplastic nodule formed by normal hepatocytes and Kupffer cells that congregate around a solid central artery
  • do not hemorrhage, are not hormonally responsive, not associated with malignant change
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26
Q

what is a hepatic adenoma?

A
  • can have malignant degeneration to HCC
  • may enlarge upon exposure to higher levels of circulating hormones
  • can contain intraparenchymal hemorrhage
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27
Q

treatment of hepatic adenoma?

A

resection if possible

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28
Q

What are the most common malignant hepatic neoplasms?

A

Metastatic tumors from the GI tract, breast and lung

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29
Q

when CAN you resect a metastatic lesion in the liver?

A

metastases from colorectal cancer

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30
Q

What are the criteria for hepatic respectability for metastatic colorectal cancer confined to the liver? (3)

A

1) unilobar or bilobar disease
2) single or multiple mets
3) remnant liver = 20-30% of original volume (equivalent of 2 segments)

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31
Q

What are the criteria for hepatic respectability for metastatic colorectal cancer w Concomitant extra hepatic disease? (3)

A
  1. Liver mets in the presence of resectable or abatable pull disease
  2. Liver mets in the presence of resectable isolated extra hepatic disease (spleen, adrenal)
  3. Liver mets in the presence of resectable invasion of adjacent structures: diaphragm and adrenal
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32
Q

What is the primary risk factor for the development of HCC?

A

cirrhosis of the liver of any etiology, most commonly men older than 40 with HCV cirrhosis

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33
Q

how can hepatocellular carcinoma (HCC) be diagnosed without a tissue sample?

A

if pt has a liver mass and an elevated AFP

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34
Q

What are the Milan Criteria?

A
  • criteria for transplantation of pets w HCC
    1. 1 tumor = 5cm
    2. 3 or fewer tumors, each = 3cm in size
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35
Q

What are 3 risk factors for cholangiocarcinoma?

A
  1. Congenital choledochal cysts
  2. Primary Sclerosing cholangitis
  3. Infection with liver fluke clonorchis sinensis
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36
Q

what is cholangiocarcinoma? 2 different subdivisions?

A

adenocarcinoma that arises from biliary ductal epithelium

  1. Intrahepatic CC- pts present later, no jaundice
  2. Extrahepatic CC- aka hilar or Klatskin tumor, presents earlier with obstructive jaundice
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37
Q

most important prognostic indicator of overall survival in extra hepatic cholangiocarcinoma?

A

radical resection ith negative surgical margins (NOT regional lymph node involvement)

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38
Q

most common cancer of the biliary tree?

A

gallbladder adenocarcinoma

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39
Q

Risk factors for gallbladder adenocarcinoma?

A
  1. Female gender
  2. Gallstones
  3. Infections: salmonella, Helicobacter in the bile
  4. Adenomatous polyps (puts with polyps >1cm should undergo chole)
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40
Q

Surgical management of gallbladder adenocarcinoma?

A
  • extensive hepatic en bloc resection in addition to regional lymphadenectomy in pts with T2 or resectable T3 disease
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41
Q

Risk factors and management of hepatic angiosarcoma ?

A

Exposure to:

  1. Vinyl chloride
  2. Thorotrast contrast material
  3. Arsenic
    - Resection is only curative treatment
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42
Q

what are the most common primary malignant liver tumors occurring in children?

A

hepatoblastomas

peak incidence 2 years old

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43
Q

management of hepatblastoma?

A
  • resection or transplantation remains the primary modalities even in children w pulmonary mets that are responsive to chemo
  • follow AFP
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44
Q

What is the embryological origin of the pancreas?

A

during 4th week of gestation: a dorsal and ventral bud

  • the dorsal bud gives rise to the majority of the pancreas
  • ventral bud gives rise to the uncinate process and a portion of the head of the pancreas
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45
Q

What are the two pancreatic ducts that form during development?

A
  1. Duct of Wirsung: main duct that connects with the CBD and drains via the major papilla
  2. Accessory duct of Santorini: empties via the minor papilla
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46
Q

Blood supply of the head and uncinate process of the pancreas?

A

anterior and posterior superior and inferior pancreaticoduodenal arteries

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47
Q

blood supply of the body and tail of the pancreas?

A

branches of the splenic and Left gastroepiploic aa

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48
Q

all venous drainage of the pancreas enters the?

A

portal vein

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49
Q

parasympathetic innvervation of the pancreas?

A

originate in vagal nuclei and travel through the posterior vagal trunk

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50
Q

what is annular pancreas?

A

normal pancreatic tissue completely surrounds the second portion of the duo
- assoc with downs syndrome, intracardiac defects and intestinal malro

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51
Q

treatment of annular pancreas?

A

duodenojejunostomy to bypass the annulus

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52
Q

what are the exocrine units of the pancreas?

A

acinar cells: 80% of the pancreas, responsible for production of enzymes

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53
Q

What are the endocrine units of the pancreas?

A

islet cells: consist of a core (beta cells) and a peripheral mantle (composed of alpha, delta and pancreatic polypeptide cells)

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54
Q

distribution of islet cells in the pancreas

A

Head = PP cells
Body/tail = alpha cells
Beta and delta cells are evenly distributed

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55
Q

what is the most potent endogenous stimulant of pancreatic bicarbonate secretion? where is it synthesized?

A

secretin: synthesized in mucosal S cells of the crypts of Lieberkuhn of the proximal small bowel
- released in the presence of luminal acid and bile

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56
Q

Function of Secretin

A

to neutralize stomach acid that enters the duodenum

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57
Q

Trypsinogen: What form is it secreted in and what is function?

A
  • trypsin(activated by enterokinase in the duo)
  • fxn: protease that activates other pancreatic proenzymes for protein digestion (chymotrypsin, elastase, carboxypeptidase A and B)
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58
Q

Lipase: What form is it secreted in and what is function?

A
  • excreted in active form

- cleaves fatty acids in preparation for gut absorption

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59
Q

Colipase: What form is it secreted in and what is function?

A
  • excreted in active form

- prevents lipase inactivation by bile acids in the duo

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60
Q

Cholesterol esterase: What form is it secreted in and what is function?

A
  • excreted in active form

- cleaves cholesterol ester bonds in preparation for fatty acid and cholesterol absorption

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61
Q

Amylase: What form is it secreted in and what is function?

A
  • excreted in active form

- Cleaves complex carbohydrates in preparation for sugar absorption

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62
Q

Three phases of digestion

A
  1. Cephalic phase: smell/taste leads to secretion of enzyme rich bicarb poor fluid
  2. Gastric phase: antral distention and protein delivery stimulate release of gastrin, acidification of the duo leads to secretin release
  3. Intestinal phase: secretin and CCK release, CCK stimulates the secretion of pancreatic enzymes from acinar cells
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63
Q

Glucagon:

cell type? Function?

A
  • alpha cells

- acts primarily on hepatocytes, raises blood sugar via gluconeogenesis, lipolysis, glycogenolysis

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64
Q

Insulin: cell type? function?

A
  • beta cells

- decrease blood sugar levels, glucose uptake at cellular level

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65
Q

Somatostatin: cell type? function?

A
  • delta cells

- inhibitor of acid production, regulates pancreatic endocrine function

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66
Q

Pancreatic Polypeptide: cell type? function?

A
  • PP cells

- decreases gallbladder and pancreatic secretion

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67
Q

Vasoactive Inhibitory Peptide (VIP): cell type? function?

A
  • Delta 2 cells

- Increases gut motility and secretion

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68
Q

Describe the following signs:
Turner’s
Cullens
Fox’s

A

Turners: flank ecchymosis
Cullens: periumbilical ecchymosis
Fox’s: ecchymosis below the inguinal ligament and/or involving the scrotum

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69
Q

Causes of Pancreatitis Mnemonic

A
I: idiopathic
G: gallstones
E: ethanol (alcohol)
T: trauma
S: steroids 
M: mumps (and other infections) / malignancy
A: autoimmune
S: scorpion stings/spider bites
H: HLD/hypercalcaemia (metabolic disorders)
E: ERCP
D: drugs
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70
Q

Two different types of amylase and where theyre secreted from

A
  1. P type: 40%, pancreas

2. S type: 60%, salivary glands, fallopian tubes, ovaries, endometrium, prostate, breast, lungs and liver

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71
Q

Describe the following signs:

  • Sentinel loop sign
  • Colon Cutoff sign
A

Sentinel: a focal jejunal ileus
Colon cutoff: transverse colonic ileus
- signs seen in acute pancreatitis

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72
Q

What is the significant of ranson’s criteria and what scores are assoc w which mortality?

A
  • 11 signs that are predictive of morbidity and mortality from pancreatitis
    7 = nearly 100%
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73
Q

Which antibiotics have good penetration of pancreatic tissue in the case of pancreatic necrosis?

A
  • Imipenem
  • Third generation cephalosporins
  • Piperacillin
  • Fluoroquinolones
  • Metronidazole
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74
Q

What are three life-threatening complications of acute pancreatitis that may require surgical intervention?

A
  1. Pancreatic abscess
  2. Infected pancreatic pseudocyst
  3. Infected pancreatic necrosis
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75
Q

What is the soap bubble sign in relation to pancreatitis?

A
  • extraluminal retroperitoneal air seen on plain films of the abdomen indicative of pancreatic infection
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76
Q

Treatment of pancreatic infectious complications with pancreatitis?

A

antibiotics and judicious surgical debridement, abscess and necrotic tissue requires debridement and wide drainage

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77
Q

Causes of idiopathic chronic pancreatitis (5)

A
  1. Social drinking
  2. Analgesic abuse
  3. Autoimmune diseases: PSC, sjogren syndrome, PBC
  4. Genetic abnormalities: cystic fibrosis and hereditary pancreatitis
  5. Pancreatic divisum
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78
Q

what gene is mutated in hereditary pancreatitis?

A

cationic trypsinogen gene

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79
Q

what can you see on pancreatogram in chronic pancreatitis?

A
  • most commonly: uniform ductal dilation

- chain of lakes characteristic

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80
Q

what is a simple test to evaluate exocrine pancreatic function?

A
  • fecal fat secretion: look for elevated fecal elastase levels (sensitive and specific for diagnosis of dysfunction)
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81
Q

endogenous enzyme secretion must be decreased by ___ to produce malabsorption?

A

90%

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82
Q

How do you manage a pt w a dilated pancreatic duct in need of operative therapy for chronic pancreatitis?

A

Puestow procedure

side-to-side pancreaticojejunostomy

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83
Q

when do you consider a pancreatic fluid collection a pseudocyst?

A

if they persist beyond 4 weeks after the onset of acute pancreatitis

84
Q

Management of pancreatic pseudocysts

A
  • trial of 6weeks of observation attempted

- surgical resection (cyst jejunostomy or cyst gastrostomy) if persistent on fu CT or persistent pain/complications

85
Q

Pancreatic Trauma Classification: Description and Treatment- Class I

A
  • Minor pancreatic contusion or superficial laceration without main ductal injury
  • observation and/or external drainage depending on whether laparotomy is warranted from other injuries
86
Q

Pancreatic Trauma Classification: Description and Treatment- Class II

A
  • Major contusion or major laceration without main ductal injury
  • Observation and/or external drainage depending on whether laparotomy is indicated for other injuries
87
Q

Pancreatic Trauma Classification: Description and Treatment- Class III

A
  • Severe parenchymal injury or main distal ductal disruption/distal pancreatic transection
  • body and tail injuries are treated with distal pancreatectomy
  • inferior head/uncinate process injuries are treated with external drainage or pancreaticojejunostomy
  • central head injuries adjacent to duo are treated like class IV injuries
88
Q

Pancreatic Trauma Classification: Description and Treatment- Class IV

A
  • severe parenchymal injury with proximal pancreatic ductal injury involving the ampulla
  • debridement and external drainage, consider pyloric exclusion and gastrojejunostomy
89
Q

Pancreatic Trauma Classification: Description and Treatment- Class V

A
  • massive disruption of the pancreatic head

- consider whipple like class IV

90
Q

which tumor suppressor genes have been implicated in the pathogenesis of pancreatic cancer? (4)

A
  1. p53
  2. DPC4
  3. k-ras
  4. BRCA2
91
Q

what is couvoisier sign?

A

the presence of an enlarged gallbladder (palpable) which is nontender + obstructive jaundice 2/2 tumors of the biliary tree

92
Q

What are the following nodes:

  1. Virchow’s
  2. Sister Mary Joseph node
  3. Blumer shelf
A
  1. Virchow: left supraclavicular adenopathy
  2. Sister mary: periumbilical lymphadenopathy
  3. Blumer: drop medastases in the pelvis palpable on rectal exam
93
Q

most common type of pancreatic cancer?

A

ductal adenocarcinoma: 65% arise in head, neck or uncinate process
15% in body or tail
20% diffusely

94
Q

acing cell carcinoma of the pancreas: describe

A

thought to results from malignant degeneration of acing cells of pancreas
- can present w subcutaneous fat necrosis, an erythema nodosum like rash, eosinophilia or polyarthralgia

95
Q

Intraductal papillary mucinous neoplasm: IPMN, describe, genetic mutation

A
  • considered a precursor lesion to adenocarcinoma
  • genetic mutations of k-ras and p53
  • mucin producing and cellular atypia
96
Q

solid pseudopapillary tumor: describe, pt population

A
  • low malignant potential
  • can grow as large as 30cm
  • females (10:1 males), pts in their mid twenties
97
Q

mucinous cystic neoplasm (MCN): describe, pt population

A
  • cystic mucin-secreting tumor
  • will likely degenerate to cystuadenocarcinoma if not resected early
  • female predominance, age 40-50
98
Q

intraductal oncocytic and papillary neoplasm (IOPN): describe

A

intraductal neoplasm similar to IPMN with slightly more malignant potential

99
Q

most common primary tumor that metastasizes to the pancreas

A

renal cell carcinoma

100
Q

pancraeticoduodenectomy is used for which pancreatic tumors?

A

tumors at the head of the pancreas

101
Q

when initially entering the abdomen for a whipple for pancreatic cancer, what factors preclude continuing on with resection? (2)

A
  1. Distant metastases to the peritoneum or liver

2. local extension to the mesenteric vessels

102
Q

what are the three anastamoses created in a whipple?

A
  1. Pancreaticojejunostomy
  2. Choledochojejunostomy
  3. Duodenojejunostomy or gastrojejunostomy (depending on whether the pylorus is preserved)
103
Q

management of biliary obstruction 2/2 unresectable pancreatic cancer?

A

hepaticojejunostomy and roux-en-y reconstruction

104
Q

what is the prevalence of pancreatic neuroendocrine tumors?

A

1% of all pancreatic tumors, 5 cases per 1 million people

105
Q

which neuroendocrine pancreatic tumor rarely has malignant potential?

A

Insulinoma (10%)

106
Q

what are the five pancreatic neuroendocrine tumors?

A
  1. Insulinoma
  2. Gastrinoma
  3. Glucagonoma
  4. VIPoma
  5. Somatostatinoma
107
Q

Whipple’s triad for insulinoma

A
  1. Hypoglycemia while exercising or fasting
  2. Plasma glucose level lower than 50mg/dL
  3. Resolution of symptoms with administration of IV glucose
108
Q

what is the most sensitive study for the localization of insulinomas?

A

endoscopic US

109
Q

What is nesidioblastosis? treatment?

A
  • nestlike increase in islet cells in children leading to hypoglycemia
  • tx: near total pancreatectomy
110
Q

what percentage of gastrinomas are associated with MEN-1?

A

25%

111
Q

diagnosis of gastrinoma? how do you localize the tumor?

A
  • serum gastrin level! if higher than 1000 then virtually diagnostic
  • confirm with secretin stimulation test, an increase in gastrin levels following a secretin bolus is a positive result
  • localize with somatostatin receptor scintigraphy, if fails then intro US and direct visualization
112
Q

symptoms of a gastrinoma?

A
  1. diarrhea
  2. peptic ulcers
  3. epigastric pain/reflux esophagitis
113
Q

what is Passaro’s triangle?

A

where the majority of gastrinomas are found, aka the gastrinoma triangle

114
Q

Treatment of gastrinoma?

A

initially: H2 blockers and PPIs

resection indicated in cases of localized disease

115
Q

What is Verner-Morrison syndrome?

A
  1. Profound watery diarrhea
  2. Hypokalemia
  3. Achlorhydria
    - caused by VIPoma, resection is considered if localized
116
Q

Glucagonoma symptoms (4)

A
  1. Erythematous skin eruptions (can become necrotic- i.e. necrolytic migrating erythema)
  2. Mild diabetes mellitus
  3. Weight loss
  4. Anemia
117
Q

treatment of glucagonoma?

A

surgical resection

skin rash can be tx with high protein diet, zinc, control of diabetes

118
Q

Symptoms of somatostatinoma?

A
  1. Steatorrhea
  2. N/v
  3. Gallstones
    - surgical resection
119
Q

hemobilia is most frequently accompanied by what other finding?

A

arterial pseudoaneurysm

120
Q

what is the triad of hemobilia?

A
  1. Hematemesis (upper GI bleeding)
  2. RUQ pain
  3. Jaundice
121
Q

what is the underlying pathology in hemobilia? treatment?

A

typically due to trauma, a pseudoaneurysm (arterial) that has a connection with the biliary tree (hence jaundice), treatment: angiographic embolization of the artery

122
Q

how do you diagnose choledochal cysts?

A

US

123
Q

treatment of choledochal cysts?

A

excising the cyst with a biliary enteric bypass (risk of malignancy increases with the more advanced age at which the cyst is detected)

124
Q

how do you repair a small lateral injury to the CBD?

A

closing the ductotomy over a T tube

125
Q

how do you repair a complete transection of the CBD?

A

biliary enteric bypass, ie hepaticojejunostomy, however if no experienced surgeon is available then drain the area, place transhepatic catheters and refer the patient

126
Q

what effect does the vagus nerve have on the gallbladder?

A

causes gallbladder contraction

127
Q

what is the management of T1 gallbladder adenocarcinoma?

A

those that are discovered incidentally and are superficial ie carcinoma in situ or T1 lesions (do not extend into perimuscular connective tissue) and have negative margins, tx = cholecystectomy alone

128
Q

management of more advanced gallbladder adenocarcinoma (T2-T4)

A

radical cholecystectomy including subsegmental resection of segments IVb and V + hepatoduodenal ligament lymphadenectomy, followed by radiation therapy postoperatively

129
Q

what 4 diseases are associated with sclerosing cholangitis?

A
  1. ulcerative colitis
  2. diabetes
  3. riedel thyroiditis
  4. retroperitoneal fibrosis
130
Q

what is the hallmark feature of emphysematous cholecystitis?

A

gas within the gallbladder wall or lumen

131
Q

what are the 4 most common pathogens associated with emphysematous cholecystitis?

A
  1. Clostridia welchii
  2. E coli
  3. Enterococcus
  4. Klebsiella
132
Q

management of emphysematous cholecystitis?

A

broad spectrum antibiotics and emergent surgery (still has a 25% mortality and 50% morbidity)

133
Q

what makes up bile?

A

80% bile salts, 15% phospholipids, 5% cholesterol

134
Q

what is the management of gallstone ileus?

A

transverse enterotomy proximal to the obstructed stone and strong removal (cholecystectomy should be reserved for you, low-risk, stable patients)

135
Q

why do u get air in the biliary tree in gallstone ileus?

A

the large gallstone erodes through the gallbladder and into the adjacent duodenum creating a cholecystoenteric fistula

136
Q

what are aschoff-rokitansky sinuses?

A

seen in chronic cholecystitis, these sinuses develop as a result of atrophy of the mucosa , the epithelium protrudes into the muscle coat leading to sinus formation

137
Q

US findings were considered positive for acalculous cholecystitis if what 3 criteria were present?

A
  1. Wall thickness >4mm
  2. hydrops
  3. sludge
138
Q

what is the most sensitive finding on HIDA scan to diagnose acalculous colecystitis?

A

failure to visualize the gallbladder

139
Q

management of acalculous cholecystitis?

A

urgent cholecystectomy unless patient is super ill then perform percutaneous US/ CT guided cholecystostomy

140
Q

whats the difference between black and brown cholesterol stones

A

black: seen in hemolytic disorders i.e. hereditary spherocytosis
brown: formed within the ducts themselves, are friable, and are assoc with parasitic infections and bacteria

141
Q

which population do you see more brown stones than black?

A

asian populations

142
Q

what is the most common cause of benign bile duct stricture?

A

ischemic from operative injury

143
Q

why do you excise a choledochal cyst?

A

because of the risk of malignancy

144
Q

what is cholesterolosis?

A

aka strawberry gallbladder caused by accumulation of cholesterol in macrophages in the gallbladder mucosa, gives the mucosa a characteristic strawberry gallbladder, benign condition

145
Q

what is a klatskin tumor?

A

perihilar cholangiocarcinomas

146
Q

what are the four types of klatskin tumors?

A
  1. Limited to the common hepatic duct
  2. involve the bifurcation of the right and left hepatic duct (type II)
    3/4. Enter into the secondary right (IIIa) or left (IIIb) intrahepatic ducts
147
Q

how do you manage type I and II klatskin tumors?

A

resection of the entire extrahepatic biliary tree with portal lymphadenectomy and bilateral roux-en-y hepaticojejunostomies, + hemihepatectomy

148
Q

how do you manage type III klatskin tumors?

A

lobectomy of liver

149
Q

what is the postulated cause of FNH?

A

an early embryologic disturbance in liver blood flow

150
Q

what are the hallmark features of FNH?

A

presence of a central scar on CT or MRI that enhances with contrast

151
Q

what is an effective screening tool for pts at high risk of developing HCC?

A

US and AFP

152
Q

what is budd chiari syndrome?

A

thrombosis of the hepatic IVC or hepatic veins themselves that leads to hepatic venous outflow obstruction, postsinusoidal liver failure and cirrhosis

153
Q

what is the classic triad of budd chiari syndrome?

A
  1. Abdominal pain
  2. Ascites
  3. Hepatomegaly
154
Q

What are the four forms of budd chiari syndrome?

A
  1. Acute
  2. Chronic
  3. Asymptomatic
  4. Fulminant
155
Q

what is budd chiari syndrome associated with?

A

Hypercoagulable state either inherited (protein C, protein S, factor V leiden) or acquired (myeloproliferative disorders, polycythemia vera, pregnancy)

156
Q

how do you diagnose budd chiari syndrome?

A

duplex ultrasound showing thrombosed hepatic veins or IVC

157
Q

what is the most prominent feature on CT scan of budd chiari syndrome?

A

caudate lobe (segment I) hypertrophy and inhomogenous contrast enhancement

158
Q

how do you distinguish FNH and hepatic adenomas?

A

sulfur colloid scan- adenomas will appear “cold” and FNHs “hot” because of presence of Kupffer cells

159
Q

what are the four types of cystic hydatid disease? and what causes cystic hydatid disease?

A

caused by tapeworm Echinococcus granulosus
Type 1: simple cyst
Type 2: hydatid sand, a cyst w free floating hyperechogenic material
Type 3: a cyst with a rosette appearance suggesting daughter cyst
Type 4: a cyst with a diffuse hyperechoic solid pattern

160
Q

what is the treatment of type I and type II hydatid cysts?

A

PAIR: percutaneous aspiration, injection of solicidal agent and reaspiration

161
Q

steps in managing ascites in cirrhosis pts?

A
  1. Low sodium diet with spironolactone and furosemide
  2. large volume (4-6L) paracentesis
  3. TIPS if good liver function
  4. liver txp if bad liver function
162
Q

what is the classic triad of pyogenic liver abscess?

A
  1. RUQ pain
  2. Fever
  3. Jaundice
163
Q

what is the most common etiology of pyogenic liver abscesses?

A

biliary tract

164
Q

treatment of pyogenic liver abscsess?

A

IV abx with percutaneous aspiration with or without catheter drainage

165
Q

the principal mediators of fibrosis leading to cirrhosis in the liver are:

A

ITO (liver stellate) cells

166
Q

esophageal varices + splenomegaly in the absence of evidence of cirrhosis (normal hepatic function), is suggestive of what?

A

Portal Vein Thrombosis!

thus perform duplex ultrasound of portal vein

167
Q

when should you selectively use preoperative biliary drainage via endoscopic retrograde cholangiopancreatography and stunting before a whipple?

A
  1. cholangitis
  2. severe intractable pruritus
    (otherwise it increases wound infections and pancreatic fistulas)
168
Q

most common polyp of the gallbladder?

A

cholesterol polyps

169
Q

what are the indications for cholecystectomy in a patient w a polyp? 4

A
  1. A symptomatic polyp
  2. A polyp in association with gallstones
  3. A polyp larger than 10mm
  4. Age older than 50
170
Q

why do you use moprhine in a HIDA scan of a pt with suspected acalculous cholecystitis?

A

it decreases rate of false positive HIDA scans bc it leads to sphincter of oddi contraction and increases the likelihood of filling of the gallbladder

171
Q

why does transecting the CBD interrupt its blood supply?

A

because the right hepatic aa and gastroduodenal aa run along the medial and lateral walls at the 3 and 9 o’clock positions

172
Q

how do you treat injuries to the distal CBD?

A

choledochoduodenostomy

173
Q

what is poland syndrome?

A

webbed fingers associated with hypoplasia of the ipsilateral pectorals mm and chest wall

174
Q

etiology of portal vein thrombosis (PVT) in adults versus children?

A

Adults: malignancy and cirrhosis
Children: neonatal umbilical vein catheterization (portal venous injury), neonatal omphalitis (umbilical sepsis), intra-abdominal sepsis (infectious seeding to portal vein)

175
Q

how does portal venous thrombosis present in children?

A

upper GI bleeding 2/2 esophageal varices, tx: octreotide and sclerotherapy

176
Q

for children with portal vein thrombosis and recurrent refractory UGI bleeding, what do you do?

A

Rex shunt: superior mesenteric vein-to-left portal vein bypass at the Rex recessus

177
Q

finding of isolated gastric varices without esophageal varices is suggestive of what?

A

splenic vein thrombosis

178
Q

most common cause of splenic vein thrombosis?

A

chronic pancreatitis (4-8% of pts)

179
Q

splenic vein thrombosis with gastric variceal formation is referred to as what?

A

left sided or sinistral portal hypertension

180
Q

anchovy paste appearance of fluid

A

amebic liver- entamoeba histolytica

181
Q

CT showing single fluid collection in the right lobe with a rim of peripheral edema

A

entamoeba histolytica liver abscess

182
Q

how do you diagnose amebic liver abscess w entamoeba histolytica? tx?

A

serologic testing using enzyme immunoassays, treat w oral metronidazole unless pt doesn’t improve within 48-72hrs then US guided aspiration

183
Q

most common benign liver tumor?

A

hemangiomas

184
Q

whats one complication of giant hemangioma in children?

A

can lead to arteriovenous shunting with CHF and thrombocytopenia

185
Q

which two methods are used to prevent first time bleeds in pts w esophageal varices?

A
  1. endoscopic ligation (superior)

2. Beta blockade

186
Q

what are the two different classifications of portovenous shunts?

A
  1. Nonselective: much more effective at decompressing portal HTN and stopping variceal hemorrhage but high risk of encephalopathy
  2. Selective: less encephalopathy
187
Q

what are the different nonselective portovenous shunts? (4)

A
  1. end to side portocaval shunt
  2. side to side portocaval shunt
  3. mesocaval shunt
  4. large diameter interposition shunts
  5. Central splenorenal shunt
188
Q

what are the selective portovenous shunts? (2)

A
  1. Distal splenorenal shunt

2. Small diameter portocaval H graft shunt

189
Q

what do you see elevated in fibrolamellar carcinoma?

A

neurotensin (NOT AFP), it also does NOT enhance on arterial phase of CT (like FNH does) nor is it hyper intense on gadolinium MRI (like FNH is)

190
Q

the hepatic veins drain which segments? right, middle, left

A

Right: V, VI, VII, VIII
Middle: IVA, IVB, V, VIII
Left: II, III
*middle and left veins join together before entering into the vena cava

191
Q

what is the round ligament of the liver and whats its significance?

A

remnant of the umbilical vein, marks the location of the intrahepatic location of the left portal vein

192
Q

what is the ligament venosum and whats its significance?

A

remnant of the ductus venosus and marks the border between the caudate lobe and the left lateral sector

193
Q

what is a replaced right hepatic artery?

A

arises from the superior mesenteric artery and is posterior to the portal vein

194
Q

what are 7 predictors of poor long-term outcome after resection of hepatic metastasis from colon cancer?

A
  1. positive tumor margin
  2. presence of extra hepatic disease
  3. node positive primary tumor
  4. disease-free interval from primary tumor to mets less than 12 months
  5. multiple hepatic tumors
  6. largest tumor >5cm
  7. CEA >200ng/mL
195
Q

most common primary liver tumor in children, what is it associated with?

A

hepatoblastoma, assoc with familial polyposis syndrome

196
Q

presentation and treatment of hepatoblastoma in children?

A

abdominal mass, anemia, thrombocytosis, elevated AFP levels, tx: chemotherapy then resection

197
Q

what are the components of CHild-Pugh?

A
Ascites (none, mild, tense)
Encephalopathy (none, stage I-II, III-IV)
Bilirubin (3)
INR (2.3)
Albumin (>3.5, 2.8-3.5,
198
Q

what is budd chiari syndrome?

A

thrombosis of the hepatic veins or intrahepatic vena cava leading to portal hypertension, jaundice from hepatic congestion

199
Q

management of budd chiari syndrome?

A

heparinization!! then portosystemic shunt

200
Q

what is the proposed etiology of FNH?

A

early embryological vascular injury

201
Q

when is portal vein embolization indicated?

A

when the remnant liver volume is expected to less than 40% with normal liver function and

202
Q

what are the three types of portal hypertension and etiologies?

A
  1. Presinusoidal: intrahepatic causes (schistosomiasis, congenital hepatic fibrosis), extrahepatic
  2. Sinusoidal: alcoholism, cirrhosis, hemochromatosis, Wilson
  3. Postsinusoidal: Budd chiari, congenital webs in intrahepatic inferior vena cava
203
Q

absolute contraindications to TIPS placement? 2

A
  1. Polycystic liver disease

2. right heart failure

204
Q

what is the ligamentum teres?

A

also known as the round ligament of the liver, its the remnant of the fetal umbilical vein

205
Q

when taking down the gastrohepatic ligament, what anomaly might you encounter?

A

a replaced left hepatic artery coming off of a left gastric

206
Q

where are most bile acids reabsorbed?

A

terminal ileum

207
Q

what is th imaging modality of choice for diagnosis and surveillance of gallbladder polyps?

A

US (MRI and CT are used to evaluate for invasion)