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Medicine 3 > Biliary Tract Disease > Flashcards

Biliary Tract Disease Flashcards

1
Q

3 categories of LFTs

A
  • Hepatocellular: Transaminase (AST and/or ALT)
  • Cholestatic: Alkaline Phosphatase
  • Bilirubin
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2
Q

Meaning of abnormal LFTs

A

-Blood tests commonly obtained to evaluate the health of the liver include liver enzyme levels, tests of hepatic synthetic function, and the serum bilirubin level. Elevations of liver enzymes often reflect damage to the liver or biliary obstruction, whereas an abnormal serum albumin or prothrombin time may be seen in the setting of impaired hepatic synthetic function. The serum bilirubin in part measures the liver’s ability to detoxify metabolites and transport organic anions into bile.

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3
Q

LFT abnormality patterns

A
  • The pattern of LFT abnormalities may suggest that the underlying cause of the patient’s liver disease is primarily the result of hepatocyte injury (elevated aminotransferases) or cholestasis (elevated alkaline phosphatase). In addition, the magnitude of the LFT abnormalities and the ratio of the aspartate aminotransferase (AST) to alanine aminotransferase (ALT) may make certain diagnoses more or less likely.
  • Hepatocellular pattern
  • cholestatic pattern
  • transaminase predominant
  • isolated hyperbilirubinemia
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4
Q

Hepatocellular pattern

A
  • Disproportionate elevation in the serum aminotransferases compared with the alkaline phosphatase
  • Serum bilirubin may be elevated
  • Tests of synthetic function may be abnormal
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5
Q

Cholestatic pattern

A
  • Disproportionate elevation in the alkaline phosphatase compared with the serum aminotransferases
  • Serum bilirubin may be elevated
  • Tests of synthetic function may be abnormal
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6
Q

isolated hyperbilirubinemia

A

As the name implies, patients with isolated hyperbilirubinemia have an elevated bilirubin level with normal serum aminotransferases and alkaline phosphatase

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7
Q

transaminase predominant pattern

A
  • most common pattern we will see in clinical practice (upper limit of normal for AST and ALT is around 40; but normal people should have levels around 10)
  • Really common to see elevations in symptomatic AND asymptomatic pts
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8
Q

Common etiologies of transaminase predominant pattern

A
  • Fatty Liver (non alcoholic – commonly associated with diabetes and metabolic syndrome) – transaminase is usually elevated but not off the charts (Their other liver tests should be pretty normal (maybe mild elevation of alk phos))
  • Hepatitis C – think about demographics and risk factors (Usually people present later in disease progression, Screen with AST)
  • Hepatitis B
  • Alcohol
  • Medications, herbal drugs, occupational toxins (NSAIDs and Tylenol) (Other meds that go through the liver for processing – makes sure to ask a good med and alcohol history )
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9
Q

uncommon etiologies of transaminase predominant pattern

A
  • Hemochromatosis (iron overload – get ferritin level)
  • Autoimmune Hepatitis – usually done by a GI specialist (Circulating autoantibodies and high serum globulin)
  • Alpha-1-AT deficiency – causes lung disease (Neonatal hepatitis)
  • Wilson’s Disease (copper accumulation due to abnormal biliary copper transport)
  • Unknown
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10
Q

AST/ALT elevation > 2:1

A

o If you see AST/ALT elevation more than 2:1, think alcohol

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11
Q

transaminase predominant: evaluation

A
  • Confirm duration >3 months (check old records)
  • R/o ETOH, drugs (IVDA), systemic illness
  • Therapeutic drug toxicity
  • Note AST/ALT ratio (AST > ALT consistent with EtOH (rarely >300); ALT > AST consistent with viral (values often >500) – ALT is SIGNIFICANTLY higher than AST)
  • Correct reversible factors: obesity, ETOH, drugs, thyroid, celiac disease
  • Abstain from Tylenol, alchohol, etc. and recheck levels in a month or so
  • Specific serological/biochemical tests: Hepatitis panel (A, B and C); Ferritin, Fe/TIBC; Copper & ceruloplasmin in young patients; Other tests as indicated by H&P, LFT’s
  • Ultrasound if suspect fatty liver, splenomegaly, or tumor/mass
  • Liver biopsy: Referral if Dx not established by above
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12
Q

Alkaline phosphate predominant: common etiologies

A
  • Metastatic or biliary Ca
  • PBC (primary biliary cirrhosis)
  • Fatty liver
  • Biliary stones
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13
Q

Alkaline phosphate predominant: uncommon etiologies

A
  • Granulomatous hepatitis (infectious, drug)

- Sclerosing cholangitis

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14
Q

Alk phos isoenzyme and GGT

A
  • Will tell you if its liver or bone
  • If GGT is elevated, it is from the liver, not bone!
  • We suggest GGT only be used to evaluate elevations of other serum enzyme tests (eg, to confirm the liver origin of an elevated alkaline phosphatase or to support a suspicion of alcohol abuse in a patient with an elevated AST and an AST to ALT ratio of greater than 2:1).
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15
Q

bilirubin predominant

A
  • rare to see ONLY bilirubin predominant
  • Fractionate bilirubin: direct and indirect
  • Hemolysis – blood cells are broken (CBC, reticulocyote count, serum haptoglobin, s/sx on PE)
  • Medications/drugs by hx and/or PE
  • Congenital hyperbilirubinemia (Gilbert’s syndrome, Dubin-Johnson)
  • Imaging if gallstones or obstruction suspected (Ultrasound, CT or MR Cholangiogram)
  • Possible referral for ERCP
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16
Q

Increase in unconjugated bilirubin

A

-An increase in unconjugated bilirubin in serum results from overproduction, impairment of uptake, or impaired conjugation of bilirubin. An increase in conjugated bilirubin is due to decreased excretion into the bile ductules or leakage of the pigment from hepatocytes into serum.

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17
Q

Increase in conjugated bilirubin

A

-An isolated elevation in conjugated bilirubin is found in two rare inherited conditions: Dubin-Johnson syndrome and Rotor syndrome. Dubin-Johnson syndrome and Rotor syndrome should be suspected in patients with mild hyperbilirubinemia (with a direct-reacting fraction of approximately 50 percent) in the absence of other abnormalities of standard liver biochemical tests. Normal levels of serum alkaline phosphatase and GGT help to distinguish these conditions from disorders associated with biliary obstruction. Differentiating between these syndromes is possible but clinically unnecessary due to their benign nature. In children, other inherited disorders caused by mutations in one of a variety of bile salt transporters may need to be considered. Patients with both conditions present with asymptomatic jaundice, typically in the second decade of life. The defect in Dubin-Johnson syndrome is altered hepatocyte excretion of bilirubin into the bile ducts, while Rotor syndrome is due to defective hepatic reuptake of bilirubin by hepatocytes.

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18
Q

Biliary tract disease

A
  • Pancreatitis
  • Cholelithiasis & Biliary Colic
  • Cholecystitis
  • Cholangitis
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19
Q

pancreatitis (acute vs chronic)

A
  • ACUTE PANCREATITIS: Inflammatory condition that occurs after an acute insult to the pancreas and resolves completely if the primary cause is eliminated; related to alcohol use, diabetes, gallstones
  • CHRONIC PANCREATITIS: Syndrome involving progressive inflammatory changes in the pancreas that result in permanent structural damage, which can lead to impairment of exocrine and endocrine function; most often from chronic alcohol use
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20
Q

etiologies of acute pancreatitis

A 
	Choledocholithiasis
	ETOH abuse
	Anatomic abnormalities
	Ampullary obstruction
	Infection
	Hypertriglyceridemia
	Hypercalcemia
	Trauma, Postoperative
	Idiopathic
	Medication reaction
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21
Q

etiologies of chronic pancreatitis

A 
	ETOH abuse
	Hereditary
	Malnutrition
	Ampullary obstruction
	Hyperparathyroidism
	Idiopathic
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22
Q

pathophysiology of pancreatitis

A

-Pancreatic enzymes released into circulation cause: Hypotension, Acute respiratory distress syndrome, Disturbance of coagulation cascade, Hypocalcemia

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23
Q

clinical features of pancreatitis

A

-Pain predominant sx
 Severe, Constant
 Epigastric or retrosternal
 Radiating to back, flank, shoulders
 Exacerbated by digestion, alcohol (which is often what put them in this place in the first place), vomiting
 Alleviated with fasting, leaning forward

24
Q

Physical exam findings of pancreatitis

A
  • Abdominal rigidity
  • Voluntary guarding
  • Fever
  • Tachycardia
  • Shock
25
Q

Dx studies of pancreatitis

A
  • abdominal plain films

- CT abdomen

26
Q

pancreatitis labs

A
  • elevated amylase and lipase (because those are made by the pancreas - when it is inflamed, makes more of the enzymes)
  • hypocalcemia
  • leukocytosis (because of the inflammation)
  • elevated BUN (dehydration or ARF) - a lot of times (due to alcohol) they are severely dehydrated
  • hyperglycemia - pancreas isnt functioning, it is inflamed
  • elevated LFTs (biliary obstruction pattern) - primarily alk phos pattern
27
Q

Outcome of pancreatitis influenced by:

A
  • etiology
  • co-morbidity (diabetes, alcoholic, etc.)
  • number of previous attacks
  • severity of disease
28
Q

complications of acute pancreatitis

A
  • Prolonged hospitalization
  • Shock
  • Hypoxia: pleural effusions, respiratory distress
  • GI bleeding
  • 25% develop pseudocysts
  • Pancreatic abscess
29
Q

chronic pancreatitis

A
  • Usually a result of chronic alcoholism
  • Complications include common bile duct or gastric outlet obstruction, ascites, and pancreatic pseudocysts
  • Symptoms usually include chronic or severe recurrent epigastric pain
  • Amylase may be elevated or normal
30
Q

chronic pancreatitis: clinical findings

A
  • Similar presentation to acute pancreatitis
  • Alcoholic patients may develop pancreatic insufficiency
  • 30% have steatorrhea due to chronic calcific pancreatitis and malabsorption
  • GI bleeding and pancreatic hemorrhage common
  • Malabsorption: emaciation, peripheral edema, multiple bruises
  • Diabetes from endocrine insufficiency
  • Jaundice suggests common bile obstruction
  • Biliary cirrhosis, cholangitis, hepatic abscess
  • Ascites/pleural effusions (leakage of pseudocyst)
  • Metastatic fat necrosis from circulating lipase
  • Polyarthritis: small joints of hands and feet
31
Q

chronic pancreatitis labs

A
  • Elevated/normal amylase, lipase
  • Hyperglycemia: advanced parenchymal damage
  • Elevated bilirubin, alk phos due to extrahepatic biliary obstruction
  • Malabsorption: hypoproteinemia, deficiency of fat soluable vitamins
  • Stool analysis for fat content
  • Ascites fluid analysis (elevated protein/amylase)
32
Q

chronic pancreatitis prognosis

A
  • Chronic pancreatitis as a primary cause of death is rare – usually they die from the complications like GI bleeding
  • Usually a consequence of associated complications: GI bleed, Biliary tract infection, Liver failure, Malabsorption, Electrolyte abnormalities
33
Q

management of chronic pancreatitis

A
  • ETOH abstinence!
  • Smaller, more frequent meals to reduce post prandial pancreatic secretions
  • Analgesics
  • Pancreatic enzymes with meals to reduce exogenous enzyme release
  • Restriction of dietary fat intake
34
Q

surgical management

A

-last resort

35
Q

biliary tract pathologies

A
  • cholelithiasis
  • cholecystitis
  • cholangitis
36
Q

cholelithiasis

A
  • 10% of US population has gallstones
  • 50% of those will be symptomatic
  • 80-90% of all gallstones are cholesterol (increased cholesterol secretion)
  • 10-20% are pigmented bilirubin (increased concentration of unconjugated bilirubin
37
Q

Cholesterol stone formation risk factors

A
  • Northern European, North/South America
  • Obesity
  • Diabetes
  • Lipid lowering drugs
  • GI disorders
  • Estrogen
  • Female
38
Q

Pigmented stone formation risk factors

A
  • asian
  • chronic hemolysis
  • alcohol cirrhosis
  • biliary infection
39
Q

cholelithiasis presentation

A
  • 18% of pts with “silent” gallstones will develop symptoms in 15-20 years
  • 3% will develop complications of biliary tract disease: cholecystitis, pancreatitis, obstructive jaundice
  • 20% of pts will discover gallstones on presentation with acute cholecystitis
40
Q

cholelithiasis

A
  • biliary colic
  • RUQ to mid-epigastric pain
  • pain is described as sharp, may be severe
  • radiates to the back/right shoulder (goes around flank, not through and through)
  • classically follows ingestions of fatty meal (1-2 hours after meal)
41
Q

cholelithiasis diagnosis

A
  • dx based on history, PE, normal labs, abdominal US
  • positive murphy’s sign is RUQ pain, cessation of breathing when you breathe in (biliary colic will have NEGATIVE murphy’s sign)
  • check LFTs, bilirubin, CBC (infection and inflammation)
42
Q

cholelithiasis management

A
  • recommend elective cholecystectomy for most patients, especially those with symptoms
  • 0.3-1% develop CA of the gallbladder (if gallbladder is calcified risk of CA is 50%)
  • non-surgical tx: 50% recurrence rate (oral bile salts slowly dissolves stones, lithotripsy, ERCP)
  • 3 methods used alone or in combination are available for the non-surgical management of patients with gallstone disease: oral bile salt therapy (primarily ursodeoxycholic acid), contact dissolution, extracorporeal shock-wave lithotripsy
43
Q

Bile acid therapy

A
  • works by inhibiting biliary secretion of cholesterol, inhibiting deposition into stones
  • reduced gallbladder wall inflammation
  • increased gallbladder emptying
  • efficacy (small stone size - <1cm, mild symptoms, good gallbladder function, buoyant stones on oral cholecystography, suggesting a high cholesterol content, minimal calcification and low density on CT imagint)
44
Q

Lithotripsy

A
  • usually recommended for patients with fewer than three stones
  • inclusion criteria for lithotripsy include: mild symptoms, normal gallbladder function with a patent cystic duct, solitary radiolucent stones, stone diameter <20mm
  • exclusion criteria include: coagulation and platelet abnormalities, cystic or vascular abnormalities of the liver, acute gallstone related complications, pregnancy
  • fewer than 20% of pts are suitable for lithotripsy
45
Q

cholelithiasis prognosis

A
  • prognosis unrelated to severity of symptoms
  • complications increase with length of time symptoms are present
  • morbidity in pts who don’t have cholecystectomy (acute colecystitis, cholangitis with liver abscess, necrotizing pancreatitis, gallstone ileus with SBO, gallbladder CA
46
Q

Acute cholecystitis

A
  • gallbladder inflammation from obstructing stone (usually)
  • hallmark is severe, constant abdominal pain (often epigastric localizing to RUQ, wraps around the flank, radiation to back, right shoulder)
  • associated with nausea/vomiting
  • exacerbation 1-2 hrs after meal
  • fever
  • RUQ tenderness, involuntary guarding
  • positive murphy’s sign (gallstones have negative murphys sign)
47
Q

Charcot’s triad

A
  • progressive infection and is considered a surgical emergency
  • RUQ pain
  • shaking chills and fever
  • jaundice (one you add jaundice, that means that there is an obstructionof the common bile duct)
  • Indicates ascending cholangitis: stasis and infection in the biliary tract
  • Considered surgical emergency
  • Antibiotic coverage for gram negatives and anaerobes
48
Q

acute cholecystitis labs

A
  • Leukocytosis
  • Elevated amylase, mild
  • Elevated ALT/AST, mild
  • Total bilirubin and Alk Phos typically not elevated
49
Q

Acute cholangitis labs

A
  • Leukocytosis with left shift (most typically bacterial infxn)
  • Elevated Alk Phos, Total (direct) bili, GGT
  • Variable elevations in ALT, AST
  • Once you start seeing a left shift, that tells you that the infection has shifted into the biliary tree
50
Q

management of acute cholecystitis

A
  • Admission
  • IV empiric antibiotics
  • Pain management
  • NPO, NG tube
  • Cholecystectomy definitive treatment (30-40% will progress to gangrenous cholecystitis and perforation without surgery)
51
Q

Primary sclerosing cholangitis

A
  • A chronic progressive disorder of unknown etiology
  • Characterized by inflammation, fibrosis, and stricturing of medium and large ducts in the intrahepatic and/or extrahepatic biliary tree
  • Complications include cholestasis and hepatic failure
  • The majority of patients with PSC have underlying ulcerative colitis (Conversely, in patients with UC, PSC occurs in approximately 5% (and perhaps less often in those with Crohn’s disease), Do not routinely screen patients with IBD for PSC, Patients with IBD who have abnormal liver tests should be evaluated for PSC)
  • they have a higher rate of developing cancer
52
Q

PSC symptoms and signs

A
  • similar to biliary tract disease
  • 50% of patients are asymptomatic at the time of diagnosis (Usually diagnosed when abnormal LFT’s are found in a patient with IBD, Fatigue, pruritus most common symptoms – especially if there is bile duct obstruction, Fevers, chills, night sweats, and RUQ pain can also be present)
  • 50% of patients have normal PE (May present with jaundice, hepatomegaly, splenomegaly, and excoriations)
53
Q

PSC evaluation

A
  • Labs show biliary pattern: elevation of Alk Phos, bilirubin; mild elevation in AST, ALT
  • Multiple autoantibodies may be positive, not specific
  • Radiographic findings include abnormal appearing bile ducts with wall thickening, dilations, and strictures
54
Q

PSC prognosis and complications

A
  • Continued destruction of bile ducts in PSC leads to end-stage liver disease
  • Patients may develop a number of other complications: Fat-soluble vitamin deficiencies (A, D, E, and K), Metabolic bone disease ,Dominant biliary strictures, Cholangitis and cholelithiasis, Cholangiocarcinoma, Gallbladder cancer, Hepatocellular carcinoma (in patients with cirrhosis), Colon cancer (in patients with concomitant ulcerative colitis)
  • There are two major goals of treatment in primary sclerosing cholangitis (PSC): Retardation and reversal of the disease process, Management of progressive disease and its complications
  • Liver transplantation is now the treatment of choice for patients with advanced liver disease secondary to PSC.
55
Q

primary biliary cholangitis

A
  • primary biliary cirrhosis

- rare t-lymphocyte-mediated attack on small intralobular bile ducts; affects women (95%) age 30-65

56
Q

recurrent pyogenic cholangitis

A

-intrabiliary pigment stone formation, resulting in stricturing of the biliary tree and biliary obstruction with recurrent bouts of cholangitis, found almost exclusively in people who live or who have lived in Southeast Asia

57
Q

Cholangiocarcinoma

A

-rare bile duct cancer, often associated with PSC, presenting with painless jaundice, right upper quadrant abdominal pain, and weight loss

Medicine 3 (11 decks)

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