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Gastrointestinal > Biliary > Flashcards

Biliary Flashcards

1
Q

Triangle of Calot is divided by the ____ artery

A

cystic

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2
Q

Bile is composed of…

A

bile salts

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3
Q

Bile salt functions to

A

aggregate around lipids to form a micelle

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4
Q

Bile is important for…

A

fat digestion and absorption

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5
Q

Fat soluble vitamins are…

A

A, D, E, K

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6
Q

Fat in the duodenum triggers…

A

release of CCK from the duodenum that causes the gallbladder to release bile

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7
Q

Gallbladder disease arises from…

A

anything that slows or prevents outflow of bile from the gallbladder.

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8
Q

What can slow/prevent outflow of bile from the gallbladder? (five things)

A
  • inflammation
  • infection
  • stones
  • stenosis
  • obstruction
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9
Q

Cholelithiasis & acute cholecystitis occurs most commonly in…

A

“fat, fertile, forty-year old, fai-haired females”

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10
Q

Cholethiasis occurs commonly due to

A

gall stones

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11
Q

Gall stone composition

A

80% cholesterol

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12
Q

Biliary colic etiology

A

spasm of the cystic duct usually from obstruction from a stone

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13
Q

What condition are you thinking when you see the following…

  • Sudden onset of pain that is constant for 1-5 hours
  • RUQ or midepigastric pain, that may radiate to R shoulder blade
  • Pain associated with fatty meals
A

Clinical presentation of biliary colic

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14
Q

Test of choice for biliary colic

A

ultrasound: see gall stones and no wall thickening or pericholecystic fluid

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15
Q

treatment of biliary colic

A
  • monitor
  • may progress to acute cholecystitis
  • elective cholecystectomy
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16
Q

Chronic cholecystitis is caused by…

A

repeated bouts of acute inflammation of the gallbladder from biliary colic or mild acute cholecystitis

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17
Q

What are the defining characteristics of chronic cholecystitis?

A

chronic inflammation can lead to calcification of the gallbladder known as a “porcelain gallbladder”

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18
Q

Etiology of acute cholecystitis

A

blockage of cystic duct, usually cholelithiasis becomes lodged in the duct

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19
Q

Acute cholecystitis mimics what other condition

A

Biliary colic, but acute cholecystitis is more severe

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20
Q

What condition are you thinking when you see the following…

  • RUQ pain radiating to right scapula
  • pain worse with movement and lasting >4 hours
  • N/V, low grade fever
  • +Murphy’s sign
A

acute cholecystitis

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21
Q

what is murphy’s sign

A

deep palpation of RUQ - positive when pain occurs with palpation that prevents a deep inspiration

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22
Q

Lab studies for acute cholecystitis:

CBC
CMP

A

CBC: leukocytosis with left shift

CMP: increased alkaline phosphate, bilirubin, ALT, AST

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23
Q

Imaging for acute cholecystisis

A

RUQ ultrasound is test of choice and see stones

CT: fat stranding (inflammation), stones, dilated duct, r/o abscess

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24
Q

Management of acute cholecystitis

Intake?
Pain management?
Surgical?
ABX?

A
  • Intake: NPO/IV fluids
  • Pain management: demerol to avoid sphincter of oddi contraction
  • Surgical: laparoscopic cholecystectomy
  • ABX: ceftriaxone and metronidazole
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25
Q

Choledocholithiasis is…

A
  • a stone in the common bile duct

- symptomatic when stone obstructs

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26
Q

What condition are you thinking when you see the following…

  • anorexia, N/V
  • light colored stools, tea-colored urine
  • jaundice
  • pruritus
A

Choledocholithiasis

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27
Q

Diagnostic gold standard for Choledocholithiasis

A

ERCP

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28
Q

Lab diagnostics of Choledocholithiasis

A

Elevated GGT

Elevated ALT, AST, ALP

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29
Q

common complication of Choledocholithiasis

A

acute pancreatitis

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30
Q

do you give Choledocholithiasis abx?

A

yes

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31
Q

Cholangitis or Ascending Cholangitis etiology

A

Infection of the biliary tree caused by stasis of the common bile duct. Stasis is usually due to stone obstructing CBD or inflation post manipulation.

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32
Q

Common infecting organisms in Cholangitis or Ascending Cholangitis

A

E. coli, Klebsiella, Bacteriodes, Enterococcus

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33
Q

Cholangitis Clinical Presentation

A

Charcot’s Triad: fever/chills, RUQ pain, jaundice

Reynold’s Pentad: fever, RUQ pain, jaundice, hypotension, mental status change

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34
Q

Charcot’s Triad

A

Cholangitis
Fever/chills
RUQ pain
Jaundice

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35
Q

Reynold’s Pentad

A 
Cholangitis: 
Fever
RUQ pain
Jaundice
Hypotension
Mental status change
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36
Q

Lab diagnostics in ascending cholangitis

CBC
LFT
Blood Cx

A

CBC: high wbc, >20K

LFT: elevated bilirubin, ALP, ALT/AST (slight)

Blood Cx: + in 50%

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37
Q

Imaging diagnostics in ascending cholangitis

A

ERCP: Visualize stone, maybe able to remove

MRCP (an ERCP with an MRI on the end)

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38
Q

How to handle “Pus under pressure” of cholangitis

A
  • Start high dose broad spectrum Abx
  • Aggressive IV fluid, thinks SIRS
  • Surgery to decompress biliary system
  • After “cooling off” patient should undergo cholecystectomy
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39
Q

Pancreatic release of enzymes is stimulated by…

A

gastric acid
CCK from duodenum
Vagal stimulation

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40
Q

Insulin is produced in…

A

beta cells of the islets of langerhans of the pancreas

41
Q

acute pancreatitis

A

inflammatory disease characterized by autodigestion of the pancreas by proteolytic enzymes, activated and produced from within the pancreases

42
Q

acute pancreatitis etiology

A

alcohol
biliary tract disease (stones blocking sphincter of Oddi most common)
hypertriglyceridemia (>500)
trauma
drugs (thiazides, estrogen, sulfonamides, slaicylates, HEART)

43
Q

Physical exam of acute pancreatitis shows…

A

fever
tachycardia
abdominal tenderness, guarding, and distention

44
Q

uncommon signs of severe necortizing pancreatitis

A

Cullen’s Sign: Periumbilical ecchymosis

Grey-Turner’s Sign: Flank ecchymosis

45
Q

acute pancreatitis laboratory diagnostics

A

CBC: leukocytosis with left shift

Elevated lipase

46
Q

why do you not give pain control in mild pancreatitis?

A

can cause sphincter of oddi contrition which increases pain/severity

47
Q

acute pancreatitis complications to be aware of

A

pancreatic abscess can lead to a pseudocyts or necrotic area that causes the pancreas to autodigest and leads to clinical deterioration

48
Q

exocrine functions of pancreas

A

releases lipase, amylase, and proteases

49
Q

endocrine functions of the pancreas

A

glucagon and insulin

50
Q

chronic pancreatitis

A

Repeated episodes of acute inflammation leading to chronic damage and ductal obstruction

51
Q

chronic pancreatitis etiologies

A

alcoholism
cystic fibrosis
idopathic

52
Q

chronic pancreatitis clinical presentation

A

epigastric pain radiating to back (aggravated by alcohol/fatty meals)
steatorrhea
malabsorption (secondary to loss of exocrine functions)
weight loss
S/Sx of diabetes (3 polys)

53
Q

3 polys of DB s/sx from chronic pancreatitis

A

polyuria
polydypsia
polyphagia (excessive hunger)

54
Q

What do you start to see on imaging with chronic pancreatitis?

A

scattered calcifications

55
Q

diagnostics for chronic pancreatitis

A

ERCP - shows chain of lakes

MRCP

56
Q

chronic pancreatitis

A

diabetes: loss of endocrine functions
steatorrhea: loss of exocrine function
pancreatic calcifications

57
Q

pancreatic carcinoma

A

95% from exocrine portion (adenocarcinoma)

75% of cancers occur in head/neck of pancreas

58
Q

Courvoisier’s Sign

A

enlarged palpable non-tender gallbladder in patients with obstructive jaundice caused by tumors of biliary tree or pancreatic head tumors

59
Q

Clinical presentation of pancreatic carcinoma

A 
early satiety/anorexia
weight loss
jaundice
abdominal pain
vague/nonspecific
courvoisier's sign
60
Q

Diagnostics of pancreatic carcinoma

A

CT scan

61
Q

Number one cause of liver failure in US

A

NASH (nonalcoholic steatohepatitis)

62
Q

NASH and alcoholic steatohepatitis

A

NASH is clinically indistinguishable from alcoholic steatohepatitis

63
Q

definitive diagnosis for NASH

A

liver biopsy showing steatosis, inflammation, cirrhosis

64
Q

progression of alcoholic liver disease

A

Alcoholic steatosis →
Steatohepatitis →
Cirrhosis →
Hepatocellular Carcinoma

65
Q

clinical presentation of alcoholic hepatitis

A

jaundice, fever, anorexia, proximal muscle wasting, hepatomegaly, tenderness to palpation over liver, bruit over liver

66
Q

Diagnostics of alcoholic hepatitis

A

liver biopsy shows mallory bodies: neutrophil infiltration into the liver & fatty changes

WBC count is normal

67
Q

unique clinical presentations of alcoholic hepatitis

A

spider angiomata

palmar erythema

68
Q

inheritance of hereditary hemochromatosis (HH)

A

autosomal recessive

69
Q

diagnostics of HH

A

genetic testing

liver biopsy with iron

70
Q

late clinical findings of HH

A

DM

71
Q

treatment of HH

A

Control diet:
Avoid iron rich foods (red meat)
Avoid acidic food (acid make iron more absorable)
Avoid Alcohol

72
Q

Wilson’s disease

A

Rare, hereditary disorder of copper metabolism that results in increased absorption and poor hepatic excretion

Autosomal Recessive

73
Q

Clinical presentation of Wilson’s Disease

A

Kayer-Flesher ring (cooper ring around cornea) and fatty infiltration of the liver leading to cirrhosis

74
Q

Diagnostics & Treatment of Wilson’s Disease

A

low serum ceruloplasmin with liver biopsy

treated with penicillamine

75
Q

Alpha-1 antitrypsin disease

A

regulates effects o neutrophil elastase produced by neutrophils in the lungs

COPD occurs at a younger age in these populations due to the destruction of the alveoli

76
Q

buildup of α-1 Antitrypsin sequence

A

Leads to hepatitis leading to cirrhosis leading to HCC

77
Q

Hepatitis A virus transmission & associated with…

A

Does not cause chronic disease or HCC

Spread via fecal-oral route

Epidemic associated with uncooked shellfish, vegetables, and fruit

78
Q

Hepatitis A clinical presentation in children

A

ASx in >90%

79
Q

Hepatitis B transmission and progression

A

Transmitted: Blood, Sexual contact, Parenteral contact

HBV is leading cause of cirrhosis and HCC (hepatocellular carcinoma) worldwide

80
Q

HBsAg

A

Positive= have virus & are chronic carriers

81
Q

HBsAb or Anti-HBs

A

Positive in vaccinated and people who have cleared the virus.

82
Q

Anti-HBc IgM

A

Indicates acute or recent infection

83
Q

HBV DNA

A

Can be quantitatively measured to obtain a viral load

84
Q

Hepatitis C

A

Most common chronic blood infection

Needles and cocaine (from the shared straw)

Sexually transmitted very rare

85
Q

Leading cause of chronic liver disease

A

Hepatitis C

86
Q

Most common cause for liver transplant

A

Hepatitis C

87
Q

Leading cause of HCC (hepatocellular carcinoma)

A

Hepatitis C

88
Q

Clinical presentation of Acute HCV

A

HVC is asymptomatic

89
Q

Clinical presentation of ChronicHCV

A

Majority are asymptomatic
RUQ discomfort
Thrombocytopenia

90
Q

HCV RNA

A

Detects the presence of virus 1-2 weeks after exposure

Determines genotype

91
Q

Hepatitis D virus

A

Patients infected with HDV are always infected with HBV

No clinical difference in patients infected with HBV or HBV+HDV.

92
Q

Cirrhosis clinical presentation

A

Fatigue, Weakness

Fluid Retention, Edema, Ascites

Dupuytren’s Contractures
(Fingers flex in)

Palmar Erythema, Spider Angiomata

Jaundice, ecchymosis

Gynecomastia, Testicular Atrophy

HSM

Abd vein dilation, Caput Medusa

93
Q

Complications of cirrhosis

A

Hepatic encephalopathy
Esophageal varices
Hepatorenal Syndrome
Spontaneous Bacterial Peritonitis

94
Q

Hepatic Encephalopathy - what is it and what are clinical manifestations

A

Bacteria in GI track produce ammonia, the liver usually detoxifies, but can’t.

Ammonia builds up and is neurotoxic.

Altered mental status, Personality changes, Obtundent, LOC, “Liver Flap”

95
Q

Esophageal Varices

- what is it and what are clinical manifestations

A

Portal vein HTN causes dilatation of veins in esophagus. If ruptures, Pt can bleed out fast and it’s difficult to control the bleeding. Bad

96
Q

Treatment for Hepatic Encephalopathy

A

Lactulose – binds NH3 and is excreted in feces (need at least three BMs a day).

Rifaximin – Non-absorbed Abx, Kills NH3 producing bacteria in GI tract

97
Q

Treatment for esophageal varices

A

Reduce portal HTN with nonselective beta-blocker (nadolol)

HR < 50

98
Q

Cirrhosis treatment

A

5:2 ratio of Spironolactone & Lasix (control ascites and hypoalbuminemia)

Nonselective Beta-blockers (nadolo, propranolol) to control portal HTN

Lactulose to control encephalopathy

ABD US Q6M screen for HCC

99
Q

HCC screening

A

Screen all cirrhotics Q6M with Abd US

No longer use AFP for screening

Gastrointestinal (12 decks)

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