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Clin Med semester 2 > Hepatobiliary part 1- Paulson-exam 3 > Flashcards

Hepatobiliary part 1- Paulson-exam 3 Flashcards

1
Q

Acute cholecystitis: Clinical presentation?

A
  • RUQ pain (or epigastric)
  • (+/-) associated NVD or fever
  • (+/-) often have a Hx of fatty food ingestion prior to presentation
  • Episode has typically lasted several hours (>4-6 hours)
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2
Q

Acute cholecystitis: Common radiation site of RUQ pain?

A
  • Right shoulder
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3
Q

Acute cholecystitis= acute inflammation of the _______

-usually characterized by?

A

gallbladder usually characterized by RUQ pain, fever, and leukocytosis with left shift (increase in bands)

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4
Q

Acute cholecystitis: Describe a positive Murphy’s sign.

A
  • PT asked to inspire deeply while examiner palpates RUQ subcostal area
  • –> inspiratory arrest and increased discomfort
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5
Q

Acute cholecystitis: Describe if providing the patients with antibiotics is a common part of the treatment plan or not.

A
  • It is often given to all patients with acute cholecystitis until clinical resolution or cholecystectomy (gallbladder removal)
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6
Q

Acute cholecystitis: Dx based on U/S findings?

A
  • Gallbladder wall thickening or edema
  • Sonographic Murphy’s sign
  • (+/-) pericholecystic fluid & dilation of the bile duct.
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7
Q

Acute cholecystitis: Empiric antibiotic treatment for community acquired acute cholecystitis of mild-to-moderate severity?

A
  • Cefazolin
  • Cefuroxime
  • (or) Ceftriaxone
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8
Q

Acute cholecystitis: Epidemiology of a calculous condition?

A
  • MC in women 40-60
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9
Q

Acute cholecystitis: Epidemiology of an acalculous condition?

A
  • MC in critically ill patients, bedridden elderly patients, and those on TPN (total parenteral nutrition)
  • 5-10% of all patients with cholecystitis
  • More prevalent in men
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10
Q

Acute cholecystitis: How long does it take for the tracer to be picked up in cholescintigraphy after injection?

A
  • Takes 30-60 minutes
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11
Q

Acute cholecystitis: How many patients present with a Hx of previous similar attacks that have resolved spontaneously?

A
  • 60-70%
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12
Q

Acute cholecystitis: How often is bacterial inflammation associated with a calculous condition?

-MC organisms?

A
  • 50-85% of PTs

- MC organisms= E. coli, Klebsiella spp, Streptococcus spp, and Clostridium spp

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13
Q

Acute cholecystitis: is an IV required for a HIDA Scan?

A
  • Yes
  • Technetium labeled HIDA injected IV–> Taken up by hepatocytes–> excreted into bile
    If cystic duct is patent, tracer enters gallbladder, which can then be visualized (takes 30-60 minutes)
    **Test is positive if gallbladder is not visualized

Note: hepatobiliary iminodiacetic acid (HIDA) scan is an imaging procedure used to diagnose problems of the liver, gallbladder and bile ducts.

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14
Q

Acute cholecystitis: Labs?

A

CBC:
- Leukocytosis with left shift (increased bands)

LFTs:
- May have mild elevation of LFTs

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15
Q

Acute cholecystitis: MC bacterial organisms associated with a bacterial inflammation in a calculous acute cholecystitis?

A
  • E. coli
  • Klbesiella spp
  • Streptococcus spp
  • Clostridium spp
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16
Q

Acute cholecystitis: On U/S, does the presence of cholelithiasis support the diagnosis of cholecystitis?

A
  • It supports the diagnosis, but it doesn’t make the diagnosis.
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17
Q

Acute cholecystitis: Other than gangrenous cholecystits, what are other complications of untreated acute cholecystitis?

A
  • Perforation
  • Cholecystoenteric fistula
  • Gallstone ileus
  • Emphasematous cholecystitis.
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18
Q

Acute cholecystitis: Other than U/S, what is another imaging modality that could be used?

A
  • HIDA Scan (Cholescintigraphy)
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19
Q

Acute cholecystitis: Pathophysiology of acalculous cholecystitis?

A
  • > 50%: no underlying explanation found.
  • (+/-) biliary sludge in the cystic duct, vasculitis, obstructing adenocarcinoma of the gallbladder, unusual infections, or systemic disease processes such as sarcoidosis, TB, syphilis.
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20
Q

Acute cholecystitis: Pathophysiology of a calculous condition?

A
  • Usuall cystic duct becomes obstructed by a stone.
  • -> Leads to inflammation.
  • Bacterial inflammation may have a role in 50-85% of patients
  • MC organisms: E. coli, Klebsiella spp, Streptococcus spp, and Clostridium spp
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21
Q

Acute cholecystitis: Physical exam findings?

A
  • Usually ill-appearing
  • Fever
  • (+/-) tachycardic
  • (+/-) voluntary and involuntary guarding or rebound tenderness
  • RUQ likely TTP
  • POSITIVE Murphy’s sign
  • (+/-) enlarged, tender gallbladder
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22
Q

Acute cholecystitis: Patients with acalculous cholecystitis usually have **underlying severe illnesses. What are some of these conditions?

A
  • Serious trauma or burns
  • Postpartum period after prolonged labor
  • Post-op after major surgery
  • Patients on TPN
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23
Q

Acute cholecystitis: (T/F) If PT is untreated, symptoms will not resolve.

A
  • False

- Symptoms MAY subside within 7-10 days

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24
Q

Acute cholecystitis: Tx?

A
  • Hospital admission
  • Pain management (NSAIDs or opioids)
  • Abx
  • Cholecystectomy or cholecystotomy
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25
Q

Acute cholecystitis: What is a positive finding associated with a HIDA scan (Cholescintigraphy)?

A
  • Test is positive if gallbladder is not visualized.
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26
Q

Acute cholecystitis: What is the most common complication if the patient is not treated?

A
  • Gangrenous cholecystitis (~20%)= MC complication**

Other complications if left untreated:

  • Perforation–> Can lead to abscess or generalized peritonitis
  • Cholecystoenteric fistula
  • Gallstone ileus
  • Emphasematous cholecystitis
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27
Q

Acute cholecystitis: What specifier is typically added to this condition?

A
  • Calculous

- Acalculous

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28
Q

Acute cholecystitis: When is a HIDA scan indicated?

A
  • If Dx is still uncertain after an ultrasound.
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29
Q

Acute cholecystitis: Why is technetium labeled HIDA utlized in a cholescintigraphy?

A
  • Taken up by hepatocytes which is then excreted into bile.

- If the cystic duct is patent, tracer enters gallbladder, which can then be visualized.

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30
Q

Anatomy: What are the ducts that originate from the liver that converge and enter the duodeunum.

A
  • Left Hepatic duct and Right hepatic duct (converge) and form the –>Common hepatic duct.
  • Common hepatic duct and cystic duct come together and form the common bile duct
  • Common bile duct & pancreatic duct go into–> Ampulla of Vater (goes into duodenum)
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31
Q

Bilirubin: Bilirubin is a product of the breakdown of what common cell?

A
  • Old/damaged RBCs
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32
Q

Bilirubin: Bilirubin that is the product from a breakdown of old/damaged RBCs forms what type of bilirubin?

A
  • Unconjugated (indirect) bilirubin.
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33
Q

Bilirubin: Conjugated bilirub is secreted from the liver into what?

A
  • Bile
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34
Q

Bilirubin: Once bile is produced in the liver, what structure does it drain into?

A
  • The biliary tree.

Summary: Bile produced in the liver–>drains into the biliary tree

  • Bilirubin is a component of bile
  • –From breakdown of old/damaged RBCs forms unconjugated (indirect) bilirubin
  • -Liver conjugates this bilirubin –> makes conjugated (direct) bilirubin–>Conjugated bilirubin secreted into bile
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35
Q

Bilirubin S/Sx: Other than jaundice, what are other common symptoms related to an increase in bilirubin?

A
  • Clay-colored stools
  • Dark tea-colored urine
  • Pruritis
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36
Q

Bilirubin: (T/F) Bilirubin is a component of bile.

A
  • True
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37
Q

Bilirubin: The biliary tree is a system of vessels that direct secretions from which organs?

A
  • Liver
  • Gallbladder
  • Pancreas
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38
Q

Bilirubin: The liver conjugates unconjugated (indirect) bilirubin to form what product?

A
  • Conjugated (direct) bilirubin.
39
Q

Bilirubin: What is the role of bile?

A
  • Emulsify fats in the GI tract–> absorbed easier
40
Q

Bilirubin: What structure conjugates the unconjugated (indirect) bilirubin.

41
Q

Bilirubin: Where is bile produced?

A
  • In the liver
42
Q

Bilirubin: Why is bile’s emulsification of fats in the GI tracts helpful for the GI system?

A
  • fats are absorbed easier.

-Bilirubin is a component of bile
–From breakdown of old/damaged RBCs forms unconjugated (indirect) bilirubin
Liver conjugates this bilirubin –> makes conjugated (direct) bilirubin
–>Conjugated bilirubin secreted into bile

43
Q

Cholecystectomy/Cholecystotomy: Emergent action is needed for patients who…

A
  • Have progressive S/Sx (i.e. high fever, hemodynamic instability, or intractable pain)
  • Suspicion for gallbladder gangrene or perforation.
44
Q

Cholecystectomy/Cholecystotomy: Proper action to take when the risks outweigh the benefits with no indication for emergent treatment?

A
  • Gallbladder drainage with percutaneous cholecystotomy
  • Resolves the acute episode in 90% of patients
  • Once acute episode resolved, reassess risk for surgery, schedule elective cholecystectomy if possible.
45
Q

Cholecystectomy/Cholecystotomy: What procedure is indicated for low-risk patients?

A
  • Cholecystectomy during initial hospitalization (laparoscopic)
46
Q

Cholecystectomy: How do most patients feel who were symptomatic with cholelithiasis after a cholecystectomy?

A
  • Most patients had symptom relief after surgery
47
Q

Cholecystectomy: Possible complications of the procedure?

-up to 12% of Pts develop ______

A
  • Bile leak
  • Bleeding
  • Abscess formation
  • Biliary injury
  • Bowel injury
  • Up to 12% of patients develop diarrhea afterwards
48
Q

Cholelithiasis: AKA?

A
  • Gallstones
49
Q

Cholelithiasis: Biliary colic may be associated with what other signs and symptoms?

A
  • NV
  • Diaphoresis

biliary colic= Pain that occurs when a gallstone is being passed and is blocking a bile duct, typically comes and goes in a fairly regular pattern

50
Q

Cholelithiasis: Black pigment stones are formed in _____

A

Sterile bile

51
Q

Cholelithiasis: Brown pigment stones are from:

A
  • bacterial metabolism in biliary infection.
52
Q

Cholelithiasis: Describe “biliary colic”

A
  • Intense, dull discomfort
  • Usually in RUQ
  • (+/-) radiate to back (esp. R shoulder blade)
53
Q

Cholelithiasis: Dx studies?

A
  • U/S

- Labs are normal (even during biliary colic)

54
Q

Cholelithiasis: MGMT for asymptomatic PTs?

A
  • Do NOT perform cholecystectomy
55
Q

Cholelithiasis: MGMT for atypical symptoms with gallstones

A
  • Lower relief rates after cholecystectomy than those with typical symptoms + stones
56
Q

Cholelithiasis: MGMT for typical biliary symptoms + gallstones?

A
  • Pain management during acute attack (NSAIDs or opioids)

- Cholecystecomy or medical dissolution of stones

57
Q

Cholelithiasis: MGMT for typical symptoms but no stones visualized?

A
  • May have a functional gallbladder disorder.
58
Q

Cholelithiasis: Patients with microlithiasis may have what kind of appearance on U/S?

59
Q

Cholelithiasis: Pigment stones can present in what colors?

A
  • Black stones

- Brown stones

60
Q

Cholelithiasis: PT demographic?

A
  • Increases after 40 YO
  • MC in women
  • Prevalent in Western countries
61
Q

Cholelithiasis: PTs are typically asymptomatic unless the condition is complicated by ______

A

obstruction/inflammation –>80% will remain asymptomatic

-If symptomatic: usually from intermittent blockage of cystic duct by a stone (Pt will have biliary colic, often assoc. with N/V and diaphoresis)

62
Q

Cholelithiasis: S/Sx?

A
  • Asymptomatic
  • Usually an incidental finding
  • Usually no positive exam findings
63
Q

Cholelithiasis: Typical duration of biliary colic?

A
  • Usually lasts at least 30 minutes, plateaus by 60, then subsides.
64
Q

Cholelithiasis: What are the “4 Fs” of cholesterol stones?

A
  • Fat
  • Forty
  • Female
  • Fertile
65
Q

Cholelithiasis: What are the two main categories of cholelithiasis?

A
  • Cholesterol

- Pigment stones

66
Q

Cholelithiasis: What often triggers biliary colic?

A
  • A fatty meal
67
Q

Cholelithiasis: What would you see on U/S?

-Labs?

A
  • **Echogenic foci that cast an acoustic shadow.
  • Gravitationally dependent
  • Those with microlithiasis may have the appearance of sludge

Labs: Normal–>Even during biliary colic

68
Q

Cholelithiasis: Which is more common in Western countries, cholesterol or pigment stones?

A
  • Cholesterol

- 90% of all gallstones in Western countries.

69
Q

Chronic cholecystitis: Describe.

A
  • Chronic inflammation of the gallbladder wall.

- Almost always associated with gallstones

70
Q

Chronic cholecystitis: How common is bacteria present in the bile of these patients?

A

> 25% of PTs

71
Q

Chronic cholecystitis: How does the presence of multiple episodes of biliary colic correlate with symptoms?

A
  • Presence does not necessarily correlate with symtpoms.
72
Q

Chronic cholecystitis: Likely etiology?

A
  • From repeated episodes of acute or subacute cholecystitis or gallstones that cause persistent irritation to gallbladder wall
  • -> fibrosis & thickening of gallbladder
73
Q

Chronic cholecystitis: S/Sx?

A

Patient may describe **multiple episodes of biliary colic

–Presence does not necessarily correlate with symptoms

74
Q

Chronic cholecystitis: Tx?

A
  • Cholecystectomy
75
Q

Chronic cholecystitis: What is a condition that is almost always associated with this?

A
  • Gallstones
76
Q

Chronic cholecystitis: What would you find on U/S?

A
  • Cholelithiasis

- (+/-) Wall thickening from scarring

77
Q

Increased conjugated (direct) bilirubin: What are intrahepatic causes of a biliary tree obstruction?

A
  • Primary biliary cirrhosis
  • Cancer
  • Granuloma
78
Q

Increased conjugated (direct) bilirubin: What are reasons or conditions that the liver wouldn’t seecrete the bilirubin into bile ducts?

A
  • Any dz that damages the liver (i.e. hepatitis, toxin- induced liver failure)
  • Dubin-Johnson syndrome
  • Rotor syndrome
79
Q

Increased conjugated (direct) bilirubin: What are the extrahepatic causes of a biliary tree obstruction?

A
  • Stones
  • Stricture
  • Cancer
80
Q

Increased conjugated (direct) bilirubin: What are the two categories of conditions that would obstruct the biliary tree?

A
  • Intrahepatic

- Extrahepatic

81
Q

Increased unconjugated bilirubin: Describe Crigler-Najjar syndrome.

A

Crigler-Najjar syndrome is a rare inherited disorder affecting the metabolism of bilirubin, a chemical formed from the breakdown of the heme in red blood cells. (prevents conjugation to direct bilirubin in the liver)

82
Q

Increased unconjugated bilirubin: Describe Gilbert syndrome.

A

Gilbert Syndrome is a mild genetic disorder in which the liver does not properly process bilirubin.

83
Q

Increased unconjugated bilirubin: What conditions lead to a decreased uptake of bilirubin by the liver?

A
  • CHF
  • Gilbert syndrome

(leads to increased unconjugated bilirubin since the liver isnt uptaking it)

84
Q

Increased unconjugated bilirubin: What conditions lead to a decrease in conjugation of bilirubin by the liver?

A
  • Crigler-Najjar syndrome

- Gilbert syndrome

85
Q

Increased unconjugated bilirubin: What hematologic disorder leads to an increased production of bilirubin?

A
  • Hemolytic anemia
86
Q

Jaundice: Comes from an increase in either…

A
  • Unconjugated bilirubin

- Conjugated bilirubin.

87
Q

Porcelain gallbladder: Describe.

-may be a form of chronic cholecystitis in >___%

A
  • Calcification of the gallbladder wall.

- May be a form of chronic cholecystitis in >95%

88
Q

Porcelain gallbladder: How is this condition typically diagnosed?

A
  • Incidentally on X-ray
89
Q

Porcelain gallbladder: How often is this condition associated with cholelithiasis?

A

> 95% of PTs

90
Q

Porcelain gallbladder: (T/F) Unlike other forms of cholecystitis, this condition is typically symptomatic.

A
  • False

- Usually asymptomatic.

91
Q

Porcelain gallbladder: These PTs are at an increased risk for what conditions?

A
  • Gallbladder carcinoma
92
Q

Porcelain gallbladder: Tx?

93
Q

Porcelain gallbladder: While this condition may be suspected incidentally on X-ray, what imaging modality would confirm the diagnosis?

A
  • U/S [OR]

- CT

94
Q

What are some major functions of the liver?

A
  • Gluconeogenesis & Glycogenolysis –> provides glucose
  • Detoxification
  • Produces bile
  • Produces proteins like clotting factors

Clin Med semester 2 (24 decks)

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