Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Surgery Clerkship > Hepatopancreaticobiliary > Flashcards

Hepatopancreaticobiliary Flashcards

1
Q

Why is biliary colic a misnomer? What is a better term?

A

Colicky pain waxes and wanes, but gallstone pain is constant, lasting from min to hours before dissipating.
Symptomatic cholelithiasis is better

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the main risk factors for developing cholesterol gallstones?

A

Female
Fat
Forty
Fertile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why is it important to distinguish between symptomatic cholelithiasis and acute cholecystitis?

A

Management: symptomatic cholelithiasis is managed as an OP with elective lap chole. Acute cholecystitis requires hospital admission, IV AB and urgent cholecystectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are key differences in history between symptomatic cholelithiasis and acute cholecystitis?

A

SC: RUQ pain that resolves min to 3-4 hours
AC: Unremitting RUQ pain > 6 hours, N/V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are key differences in PE between symptomatic cholelithiasis and acute cholecystitis?

A

SC: Mild RUQ tenderness to palpation
AC: Murphy’s sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are key differences in vitals between symptomatic cholelithiasis and acute cholecystitis?

A

SC: normal
AC: Fever, tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are key differences in labs between symptomatic cholelithiasis and acute cholecystitis?

A

SC: normal WBC
AC: Elevated WBC with left shift

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are key differences in US findings between symptomatic cholelithiasis and acute cholecystitis?

A

SC: Gallstones
AC: Gallstones, GB wall thickening > 4mm, pericholecystic fluid, sonographic Murphy’s sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the significance of RUQ pain + scapular pain in GB disease?

A

GB and scapula share same cutaneous dermatome: scapula receives cutaneous innervation from supraclavicular nerves: same STT pathways activated!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Murphy’s sign?

A

When RUQ palpated, patient ceases inspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is significance of Murphy’s sign?

A

Specific to acute cholecystitis: represents focal peritonitis of anterior abdominal wall parietal peritoneum due to inflammation of adjacent gallbladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Characterize somatic and visceral pain?

A

Somatic: well localized, secondary to peritoneal irritation
Visceral: difficult to localize: due to mechanical stretching of visceral organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is chronic cholecystitis?

A

Recurrent bouts of symptomatic cholelithiasis: cause chronic inflammation of GB with fibrotic changes on history consistent with “chronic cholecystitis”
* Biliary colic, symptomatic cholelithiasis and chronic cholecystitis are interchangeable terms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What exactly causes acute cholecystitis?

A

Sustained obstruction o the cystic duct (by a gallstone usually). This leads to inflammation and edema of the GB wall and eventually bacterial overgrowth and invasion of GB wall. Can lead to ischemia, necrosis and rarely GB perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are typical organisms in bile in acute cholecystitis?

A

E. coli, Bacterioides, Klebsiella, Enterobacter, Enterococcus, Pseudomonas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 3 components of bile?

A

Bile salts
cholesterol
Lecitihin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How to cholesterol gallstones form?

A

Concentration of cholesterol in bile exceeds its solubility: causes precipitation of cholesterol crystals. (Due to low concentration of bile salts or lecithin, or higher levels of cholesterol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the dark color in pigmented stones comprised of?

A

Calcium bilirubinate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are black pigmented gallstones associated with? What is the black pigment composed of, and where are they found?

A

Hemolytic disease: hereditary spherocytosis or sickle cell.

Composed of unconjugated bilirubin in the GB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are brown pigmented gallstones associated with? Where are they found?

A

Associated with bacterial infection and parasites.

Found in the bile ducts where they form, more common in Asian countries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is choledocolithiasis?

A

Obstruction of CBD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is cholangitis?

A

Obstruction of common bile duct
bacterial overgrowth
infection of the entire biliary tree which ascends into liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is acute gallstone pancreatitis?

A

Obstruction of the common bile duct and pancreatic duct causing pancreatic enzyme release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is Mirizzi’s syndrome?

A

Large gallstone impacted in the cystic duct, compressing the common hepatic duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the next step in the work-up for suspected acute cholecystitis?

A
  1. RUQ US to look for:
    gallstones
    GB thickness (>4mm)
    Pericholecystic fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is sonographic Murphy’s sign?

A

Direct pressure to RUQ by US probe when patient inspires, and pain causes cessation of inspiration. More specific!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is a normal CBD diameter? Dilated?

A

Normal 4-5mm

CBD > 6mm considered abnormally dilated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How accurate is US to detect gallstones in GB vs. CBD?

A

GB: > 95% sensitive and 97% specific
CBD: Sensitivity of only 50% since bowel gas interferes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What if US shows gas bubbles in GB wall?

A

Concern for emphysematous cholecystitis: GB infected with gas forming organisms causing a necrotizing soft-tissue-like infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Who get emphysematous cholecystitis?

A

Older men with diabetes mellitus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What labs should be sent in presence of RUQ and epigastric pain? Why?

A 
Total/direct bili
AST
ALT
Alk phos
GGT
To rule out other conditions like hepatic disease, pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the proper tests for synthetic liver function?

A

Serum albumin
PT
INR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What if acute cholecystitis is suspected but US does not demonstrate gallstones?

A
  • False negative US with very small stones or very few

- Acalculous cholecystitis in critically ill patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What causes acalculous cholecystitis?

A
  • Biliary stasis + GB ischemia with severe illness

- TPN associated with it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the next step if gallstones aren’t seen on US but biliary disease is suspected?

A

HIDA scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How do we treat acalculous cholecystitis?

A

Emergent cholecystectomy or cholecystostomy tube to decompress GB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

With a patient with clinically confirmed acute cholecystitis, how to manage?

A
  1. Admit
  2. NPO
  3. IV fluids and IV antibiotics for gram negative and anaerobic coverage
  4. Lap chole w/in 48 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are best antibiotics for acute cholecystitis?

A
  • 2nd gen
  • cephalosporins
    broad spectrum penicillin/beta lactamase inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Do incidental gallstones require surgery?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is major complication of lap chole that is most common in setting of acute cholecystitis?

A

CBD injury: higher risk in men and during surgery for acute cholecystitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How to manage injury to the CBD during GB surgery?

A

<50% injury: primary via stent
>50% injury: loop of jejunum brought up to anastomose to proximal end of bile duct. Don’t attempt primary repair: could form ischemic stricture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How does CBD injury manifest when it isn’t recognized until late?

A

ab pain, bloating, anorexia and elevated LFTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How do we work up suspected delayed CBD injury?

A
  1. US and/or CT
  2. Sepsis?
  3. If no: HIDA scan
  4. If bile leak or no flow to duodenum: ERCP
    (See flow chart page 162)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is differential if lap chole patient develops RUQ pain several weeks after operation?

A 
Post-cholecystectomy syndrome:
1 residual stone in CBD
2 gallstone in cystic duct stump
3 dysfunction of biliary tree
4 Gastritis, PUD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the work-up for RUQ pain several weeks after lap chole?

A

CBC
Liver function tests
RUQ US
ERCP if needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is ideal timing for cholecystectomy for patient with acute cholecystitis?

A

< 48 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

When should acute cholecystitis be managed non operatively?

A

Critically ill patients may have too much operative risk

- if patient doesn’t improve with AB alone, place a percutaneous cholecystectomy tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

When to suspect gangrenous cholecystitis?

A 
Severe, unrelenting abdominal pain
High fever
Persistent tachycardia
Markedly elevated WBC
Hyponatremia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the key symptoms associated with cholangitis?

A

Charcot’s triad: RUQ pain, jaundice, fever

Reynolds pentad: plus AMS and hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the treatment for cholangitis?

A

Immediate decompression of biliary tract (ERCP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the definition of SIRS?

A

2+ of the following:

  1. T > 100.4 or < 98.6
  2. HR >90
  3. RR > 20 / PaCO2 < 32 or mechanically vent
  4. WBC > 12 or < 4 or > 10% band forms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

When does SIRS become sepsis?

A

When there is an identifiable source of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the diagnostic criteria for cholangitis?

A

Tokyo guidlines:

  1. Evidence of systemic inflammation (fever/leukocytosis)
  2. Cholestasis (jaundice and/or abnl liver enzymes)
  3. Biliary obstruction (dilated bile ducts on US)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the causes of obstructive jaundice that lead to cholangitis?

A 
MC: gallstones
Bile duct strictures
Parasites (Ascaris, Clonorchis sinensis)
Instrumentation of biliary tract (ERCP)
Indwelling biliary stents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

When do we expect pale stools?

A

Prolonged biliary obstruction (NOT with gallstone cholangitis: too short)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

At what level of bilirubin will jaundice first be visible? What is normal?

A

> 2.5 mg/dL

Normal up to 1.0 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Where is jaundice first visible, and where does it progress?

A

First: sclerae of eyes and under tongue because BV more superficial!
Then: chest, abdomen, legs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is Charcot’s triad? What is it classically associated with?

A

Fever
RUQ
jaundice
Cholangitis!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What percent of patients with cholangitis present with Charcot’s triad?

A

40-50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is Reynolds pentad? What percent of cholangitis patients have it?

A

Charcot’s triad + hypotension + AMS.

Only 5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How can elderly patients present with cholangitis?

A

Asymptomatically until in septic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the mortality associated with cholangitis? Who dies?

A

5%: hepatic abscesses or if original biliary obstruction secondary to malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Why are gallstones MCC of obstructive jaundice with cholangitis?

A

Need biliary obstruction + bacteria in bile. Gallstones MC because perfect vehicles to harbor bacteria in biliary tree! As the stone passes from GB: get trapped in distal CBD to harbor infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are potential consequences of unrecognized acute cholangitis?

A

Severe sepsis
Hepatic micro abscess
death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are key differences in labs between hepatic and post hepatic jaundice?

A

Hepatic: Disproportionate rise in ALT/AST
Posthepatic: disproportionate rise in alk pos and GGT (confirm liver, not bone!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is imaging test for cholangitis?

A

RUQ US to look for dilation of CBD

*But - it is bad at seeing stones in CBD!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is normal CBD diameter?

A

<4mm until age 40, then 1mm for every 10 years over 40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the 3 most important management steps after identifying SIRS?

A
  1. Aggressive fluid resuscitation
  2. Obtain blood cultures
  3. Broad spectrum antibiotics w/in 1 hour (cover enteric organisms)
  4. Coagulation studies due to increased risk of bleeding
69
Q

Where to admit patient with cholangitis?

A

ICU: hemodynamic monitoring/vasopressors if need hemodynamic support

70
Q

Once patient is stabilized, what intervention is recommended for cholangitis?

A

Drain infected bile by biliary decompression: in order of preference:

  • ERCP
  • percutaneous trans hepatic drainage
  • T-tube drain into CBD
71
Q

What is definitive management for cholangitis after biliary decompression?

A

Lap chole to prevent future episodes

72
Q

Why do cholangitis patients not get surgery immediately?

A

High morbidity/mortality bc septic patient subjected to general anesthesia / open procedure

73
Q

In an elderly patient with AMS or hypothermia alone, what should we always look for?

A

Send LFTs since cholangitis can easily be missed

74
Q

What to consider in a patient with bloody diarrhea and cholangitis?

A

UC with primary sclerosing cholangitis: inflammation and fibrosis of intrahepatic and extra hepatic bile ducts

75
Q

What does ERCP show in a patient with primary sclerosis cholangitis?

A

beaded appearance of pearls on a string

76
Q

Why can acute cholangitis be missed in elderly and immunosuppressed?

A
  • No fever or pain
77
Q

What is the differential for epigastric abdominal pain?

A 
Gastroenteritis
Acute gastritis
Acute cholecystitis
PUD
Perforated ulcer
Pancreatitis
Appendicitis
SBO
Mesenteric ischemia
Ruptured AAA
MI referred pain
78
Q

How to diagnose acute pancreatitis?

A

Clinically: 2/3:

  1. Sudden, severe persistent epigastric pain radiating to back
  2. Elevated lipase or amylase to 3x normal
  3. Characteristic imaging: enlarged pancreas, sentinel loops, colon cutoff sign
79
Q

What non surgical conditions can mimic an acute abdomen?

A 
Gastroenteritis
Acute adrenal insufficiency
sickle cell crisis
DKA
Acute porphyria
PID
Nephrolithiasis
Pyelonephritis
80
Q

What is Grey Turner’s sign and what does it indicate?

A

Blue-black discoloration in flanks: retroperitoneal hemorrhage due to acute pancreatitis

81
Q

What is Cullen’s sign and what does it indicate?

A

Blue-red discoloration at the umbilicus: digested blood products in retroperitoneum forming methemalbumin that then travel to anterior abdominal walls

82
Q

What is first step in evaluation for gallstones?

A

abdominal US

83
Q

What are the signs and symptoms of acute pancreatitis?

A

Epigastric pain radiating to the back (worsened with food)
N/V
Anorexia / decreased oral intake
PE: fever, tachycardia, epigastric tenderness w/ localized guarding, hypoactive bowel sounds

84
Q

What are the structures in the retroperitoneum?

A 
SAD PUCKER:
Suprarenal (adrenals)
Aorta
Duodenum (2/3)
Pancreas
Ureter
Colon (asc/desc)
Kidneys
Esophagus
Rectum
85
Q

What is the pathophysiology of pancreatitis?

A

Inappropriate activation of pancreatic enzymes leading to peripancreatic inflammation. Enzymes primarily damage peripancreatic tissues and vasculature: inflammatory response is out of proportion to insult, with time: damage leads to fluid sequestration, fat necrosis, vasculitis and hemorrhage

86
Q

What are etiologies for pancreatitis?

A 
GET SMASHED:
Gallstones (40%)
Ethanol (30%)
Tumors
Scorpion stings
Mycoplasma/mumps
Autoimmune (SLE)
Surgery / trauma
Hyper lipidemia/calcemia
Embolic / ischemic
Drugs / toxins
87
Q

What meds can cause pancreatitis?

A 
furosemide, thiazides
Sulfasalazine, ASA
Azathioprine
Valproate
Exenatide
Didanosine, pentamidine
88
Q

How do gallstones cause acute pancreatitis?

A

Gallstone passes into CBD and has transient impaction at ampulla: increases pancreatic duct pressure and causes reflux of duodenal juices and bile into the pancreatic duct

89
Q

In gallstone pancreatitis, how often does the gallstone remain impacted in distal CBD?

A

Not often: usually passes into duodenum shortly after impaction: ERCP not needed!

90
Q

How does alcohol cause acute pancreatitis?

A
  • Usually only after many years of abuse: intra-acinar activation of proteolytic enzymes necessary.
  • Ethanol metabolism byproducts: pancreatic hypoxia and oxidative damage
  • Excessive increase in Ca ion ccn in pancreatic cells
  • Overtime: sensitizes cells to respond to CCK prematurely: leading to inappropriate activation of zymogens in cells
91
Q

What are the key labs in acute vs. chronic pancreatitis?

A

Acute: high amylase and lipase
Chronic: low fecal elastase levels

92
Q

What are the key radiologic findings in acute vs. chronic pancreatitis?

A

Acute: dilated loops of bowel near pancreas (sentinel loops) on plain films
Chronic: pancreatic calcifications on plain films

93
Q

How many phases are there in acute pancreatitis?

A

3:
1 Premature activation of trypsin within pancreatic acing cells
2 Intrapancreatic inflammation
3 Extrapancreatic inflammation (affects multiple organ systems)

94
Q

How do we classify pancreatitis severity?

A

Mild: resolves 2-5 days
Severe: development of complications

95
Q

How do we define organ failure?

A

1 Shock < 90 systolic
2 PaO2 < 60
3 Creatinine > 2 after rehydration
4 GI bleeding > 500cc after 24 hours

96
Q

What is the mechanism for hypotension in pancreatitis?

A

Inflammation causes endothelial injury –>
1 increased permeability in peripancreatic vasculature–> fluid leaks into retroperitoneal space
2 Vasodilation –> hypotension

97
Q

What are pulmonary complications of acute pancreatitis?

A

Pleural effusions

ARDS

98
Q

How does pancreatitis cause pleural effusion?

A

Inflammation can obstruct lymph drainage around diaphragm: collection of lymph fluid travels across the diaphragm pores and into ipsilateral base on lung

99
Q

How does pancreatitis cause ARDS?

A

Severe inflammation can contribute to fistula formation between pancreatitis and thoracic cavity: free flow of pancreatic enzymes into the lungs

100
Q

What is the predominant histopathologic type of pancreatitis?

A

enlargement of pancreas due to inflammatory edema: no destruction of pancreatic cells or inflammation

101
Q

What is necrotizing pancreatitis? What is the mortality?

A

Necrotic pancreatic parenchyma: can lead to sepsis in over half of cases
17% mortality

102
Q

What are the Ranson criteria used for in acute pancreatitis?

A

Predict severity based on parameters at admission and 48 hours later

103
Q

Do amylase and lipase elevation correlate with the severity of acute pancreatitis?

A

NO

104
Q

What is the main drawback of the Ranson criteria?

A

By 48 hours, most patients have declared themselves as to whether their course will be mild or severe

105
Q

Why does hypocalcemia occur in setting of pancreatitis?

A

FFA generated by pancreatic lipase: chelate calcium salts in the pancreas, leading to saponification (deposition of Ca soaps in retroperitoneum)

106
Q

What is the natural disease course of acute pancreatitis?

A

Recover in < 5 days

107
Q

What is most common cause of mortality in first week of acute pancreatitis?

A

1st week: multi organ failure due to severe systemic inflammatory response

108
Q

What is most common cause of mortality after the first week of pancreatitis?

A

Sepsis due to pancreatic necrosis of peripancreatic abscess. MUST drain abscess to reduce mortality!

109
Q

What are key labs to order when suspecting acute pancreatitis?

A 
Amylase/lipase
LFTs
Electrolytes
CBC
Lipid panel - rule out hyperlipidemia as cause
110
Q

In patients with hemorrhagic pancreatitis, what is an important marker that can be falsely reassuring?

A

Hematocrit: can take 1-2 days to equilibrate. plus dehydration can hemoconcentration: falsely elevated or nl!

111
Q

What is the diagnostic imaging of choice for acute pancreatitis?

A

RUQ US bc gallstones are MCC

112
Q

What else can cause high amylase, besides pancreatic disease?

A 
Salivary disease (parotitis)
GI disease 
Gyn disease
Neoplasms
Renal failure: amylase really cleared
113
Q

What are classic abdominal XR findings in acute pancreatitis?

A
  1. Sentinel loop: dilated loops of small bowel in LUQ near pancreas
  2. Colon cutoff sign: distended proximal colon w/ abrupt collapse in LUQ at splenic flexure
    + Due to local ileus from pancreatic inflammation
114
Q

What is classic CXR finding in acute pancreatitis?

A

Pleural effusion: Left side

Strongly assoc w severe pancreatitis (85% patients have it)

115
Q

What is role of CT scan in evaluation of acute pancreatitis?

A

None - only use when diagnosis is in doubt

116
Q

When do we use CT for pancreatitis?

A

If patient is not clinically improving after several days of conservative management

117
Q

When is ERCP used in gallstone pancreatitis?

A

Only if suspected concomitant acute cholangitis

118
Q

What is initial management for acute pancreatitis?

A

Supportive: IVF, NPO, analgesics, NGT if vomiting

119
Q

Why do some clinicians prefer meperidine vs. morphine for pain control in acute pancreatitis?

A

Meperidine does not contract sphincter of Oddi (morphine does)
BUT: it also increases risk of seizures

120
Q

What is subsequent management of pancreatitis after supportive care?

A

If gallstones: cholecystectomy to reduce recurrence

If alcohol: counsel on cessation

121
Q

How does severity of pancreatitis affect management?

A
  1. Location of bed in hospital
  2. If severe: raises awareness for close monitoring
  3. Gallstone: assist in timing of cholecystectomy
122
Q

What to suspect: severe acute pancreatitis patient develops fever + leukocytosis 3 weeks into hospitalization?

A

Pancreatic abscess

123
Q

What to suspect: recently pancreatitis patient comes in 4 weeks later with persistent abdominal pain, palpable epigastric mass and persistently elevated amylase? How do we test for it?

A

Pancreatic pseudocyst: test with CT scan.

124
Q

What is management for pancreatic pseudocyst?

A

Most resolve w/in 6 weeks with supportive treatment.

  • Intervene if > 6cm or persists > 6 weeks or symptomatic
  • Do internal drainage: connect cyst and adjacent intestine
125
Q

What is timing of cholecystectomy in mild vs. severe gallstone pancreatitis?

A

Mild: w/in 48-72 hours
Severe: weeks later

126
Q

What are the complications of chronic pancreatitis?

A

1 Diabetes: destruction of beta-islet insulin-producing cells
2 Steatorrhea
3 Chronic pain

127
Q

What is the most common indication for surgical management in chronic pancreatitis? What is done?

A

Severe and persistent pain: place stent in pancreatic duct to improve pancreatic juice flow

128
Q

Should prophylactic antibiotics be administered for sever acute pancreatitis?

A

No: inflammation, not infection

129
Q

In a patient with HTN on HCTZ, what to consider as cause for pancreatitis?

A

Hypercalcemia: can cause secretory block in pancreatic duct. Patient may be normocalcemic since pancreatitis causes hypocalcemia.

130
Q

What are the complications of pancreatitis: early and late?

A

1st week: Development of systemic complications (organ failure)
3 weeks plus: pancreatic complications (pseudocyst, abscess, necrosis

131
Q

If a pancreatitis patient does not clinically improve within 3 days of conservative management, what is the next step?

A

Get CT scan with contrast to look for underlying complications

132
Q

In patients with prolonged NPO status due to acute pancreatitis or their condition is severe, what should be done about nutrition?

A

Begin enteral nutrition

133
Q

What is the differential diagnosis of jaundice in terms of location?

A

Preheptic/hemolytic
Intrahepatic/hepatocellular
Posthepatic

134
Q

What is in the differential for prehepatic jaundice?

A

Hemolytic anemia

Gilbert’s

135
Q

What is in the differential for hepatic jaundice?

A 
Ischemic liver injury
Viral
Toxic ingestion
Primary biliary cirrhosis
Primary sclerosing cholangitis
Wilson's disease
136
Q

What is in the differential for posthepatic jaundice?

A 
Choledocholithiasis
Acute cholangitis
Chronic pancreatitis
Mirizzi syndrome
Pancreatic carcinoma
Ampullary carcinoma
Cholangiocarcinoma
137
Q

What is Courvoisier’s sign?

A

palpable RUQ mass = non tender, enlarged GB which signifies obstruction of CBD. Associated with malignancy

138
Q

What is the implication of painful vs. painless jaundice?

A

Painful: gallstone obstruction
Painless: insidious obstruction, associated with malignancy

139
Q

What are the risk factors for pancreatic cancer?

A 
Chronic pancreatitis
Tobacco
High fat diet
Male gender
Family history
Recent onset DM
140
Q

What are the risk factors for cholangiocarcinoma?

A

UC/primary sclerosis cholangitis

141
Q

What are the risk factors for adenocarcinoma of the GB?

A

Long standing gallstone disease

142
Q

Where is jaundice best detected?

A

Mucous membranes of mouth
Palms/soles
Sclerae
* places not exposed to sunlight: more bilirubin due to lack of photodegeneration

143
Q

What is a sister Mary Joseph nodule?

A

Periumbilical mass: possible metastatic abdominal or pelvic malignancy (usually stomach, pancreatic)

144
Q

What is Blumer’s shelf?

A

Step-off felt during rectal exam: suggests metastatic disease to pouch of Douglas. Usually mets from lung, pancreas, stomach cancer

145
Q

What is the mechanism behind “clay colored stools”?

A

Biliary obstruction decreases bilirubin in intestines: decreasing stercobilin and causing clay-colored stools

146
Q

In a patient with obstructive jaundice, what labs are characteristic?

A

Elevated T bili

Elevated alk phos

147
Q

What initial imaging for painful jaundice?

A

RUQ US

148
Q

What is the imaging recommendation for painless jaundice?

A

triple phase abdominal CT: contrast during:

  1. Arterial phase
  2. Early venous phase
  3. Late venous phase
    * Detect pancreatic and periampullary masses to provide information about its respectability
149
Q

What is the role of MRCP and ECRP in evaluation for jaundice?

A

Only if no mass is seen and cause of biliary obstruction is unclear!

150
Q

What is the role of CA 19-9 and CEA in pancreatic cancer?

A

Not for screening: can use for monitoring or prognostication if malignancy is suspected.
CA 19-9: pancreatic
CEA: colorectal cancer

151
Q

What makes pancreatic cancer unresectable?

A

1 Tumor invasion into SMA, celiac or hepatic arteries

2 Metastatic disease

152
Q

Do we biopsy a resectable pancreatic mass?

A

No: just resect!

153
Q

What is the the role of preoperative stunting in presence of pancreatic mass with obstructive jaundice?

A

No benefit

154
Q

What is the role of neoadjuvant therapy for pancreatic adenocarcinoma?

A

Only to shrink “borderline resectable” tumors to make them resectable

155
Q

What is the surgical management of pancreatic or periampullary cancer?

A

Whipple procedure: pancreaticoduodenectomy. If it is resectable!

156
Q

What other conditions besides pancreatic cancer is a Whipple performed?

A

Cancer of duodenum, cholangiocarcinoma and ampullary carcinoma

157
Q

In non-resectable pancreatic tumors, what conditions warrant palliative procedures?

A

Chronic abdominal pain
Gastric outlet obstruction
Symptomatic biliary obstruction

158
Q

What is the most common complication from a Whipple?

A

Gastroparesis: treat with metoclopramide

159
Q

Is there a high risk of diabetes after a Whipple?

A

Only if patient had elevated glucose before the procedure

160
Q

When to suspect a pancreatic or biliary leak after a Whipple?

A

Look at drain:

  • Sanguinous drainage: hemorrhage
  • green drainage: biliary leak
  • Milky-gray white fluid with a sheen on bulb: pancreatic leak (will have high amylase)
161
Q

What is a non-specific clinical sign of post-operative (Whipple) leak?

A

tachycardia

162
Q

How can pancreatic cancer cause increased INR?

A

Need bile for vitamin K absorption

163
Q

How to treat increased INR from biliary tract obstruction/pancreatic cancer?

A

Parenteral vitamin K

FFP

164
Q

If a stricture is seen in the biliary tree without a mass, what diagnostic step should follow?

A

FNA or biopsy

165
Q

If a periampullary mass is unresectable, what are the next treatment options?

A

Biliary stent
Palliative chemotherapy
Surgical bypass (biliary and intestinal)

166
Q

How do we treat a borderline resectable periampullary mass?

A
  • Consider neoadjuvant chemotherapy

- Repeat imaging to assess for surgical intervention

167
Q

What labs for suspected periampullary / pancreatic mass?

A

LFTs: Bili, AST, ALT, ALP

Amylase/Lipase to rule out pancreatitic

168
Q

What are the 3 most common causes of malignant biliary obstruction?

A

Pancreatic cancer
Cholangiocarcinoma
Ampullary carcinoma

Surgery Clerkship (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions