biliary tract Flashcards
Hepatocellular pattern
Transaminase (AST and/or ALT)
usually when you have an elevation of ALT or AST you also have an elevation of ______ as well
bilirubin
MC Type of pattern you’ll see
transaminase dominant
upper limit of normal AST ALT
40
Normally b/w 15 and 20
fatty infiltration into liver that results in mild elevation of transaminases
fatty liver disease
other liver function tests should be normal
chronic hep b and C you see
asymptomatic pt
screen with ALT transaminase level and look for elevation
medications that can elevate transaminases
(Tylenol, Rifampin, INH, Antifungals, Methotrexate, NSAIDS),
Herbal drugs, occupational toxins
usually anything that utilizes the CYP450 system
uncommon etiologies for pts with transaminase predominant panel
Hemochromatosis (iron OVER)
Autoimmune Hepatitis
Alpha-1-AT deficiency
Wilson’s Disease (COPPER)
Unknown causes
Autoimmune Hepatitis can be diagnosed with
circulating autoantibodies and high serum globulin
” Alpha-1-AT deficiency is seen in what population
deficiency (rare; neonatal hepatitis)
” Wilson’s Disease is due to
rare; copper accumulation due to abnormal biliary copper transport
AST predominant ratio
ETOH-related hepatitis,
cirrhosis due to viral hepatitis,
Wilson dz
ALT predominant
usually all other casues of liver dz (not alcohol)
drug-induced liver, chronic viral hepatitis (B&C), occupational, toxin related hepatocellular damage, autoimmune hepatitis, Wilson’s, Hemochromatosis, Alpha-1-AT deficiency, congestive hepatopathy, Malignant infiltration of the liver
you want to confirm the elevation of transaminases for at least how long
> 3mo
AST>ALT
- AST>ALT consistent w/ ETOH (rarely >300)
ALT>AST consistent
consistent w/ viral (values often >500 greater than hepititis
correlative factors with elevated transaminases
Correct reversible factors: obesity, ETOH, drugs, thyroid, celiac dz
mild elevation recommendations
abstain from alcohol and medication recheck in 2 months
what to do if you suspect if suspect fatty liver, splenomegaly, or tumor/mass
ULS- can see fatty infiltration
right upper quadrant
also done with biliary tract dz
what to do if it looks like they have hep c
Hepatitis panel (A, B, C)
elevated hematocrit or signs and symptoms of hemachromatosis
Ferritin, Fe/TIBC
what to do if you suspect Wilsons
Copper & ceruloplasmin in young patients
when would you do a liver biopsy
if no other source can be ascertained
primarily alk phos is made
in liver and bones
if you don’t have any signs or symptoms of biliary tract disease and you have a high alk phos
might be coming from somewhere else need to evaluate alk pho iso enzyme
Based on alk phos isoenzyme, it will tell you the origin of Alk Phos-liver or bone
GGT will be coming from the liver
common etiologies of elevated Alk Phos
Metastatic or biliary Ca
PBC (primary biliary cirrhosis)
Fatty liver (mild elevation of Alk Phos and mild elevation of transaminases)
Biliary stones
Pt’s w/ bone cancer will show elevation in
- Pt’s w/ bone cancer will show elevation in Alk Phos
ULN for alk phos
Upper limit normal is 150
what population do you normally see an elevated alk phos
kids
can be around 400
also pregnant women
GGT increased will tel you the elevated alk phos will
. So if you have elevated Alk Phos and an elevated GGT then you know the problem is in the liver
elevated alk phos and GGT increased what do you do
RUQ ULS
what are you looking for with a ULS if you know alk phos elevation is coming from the liver
dilated biliary ducts
why would you see an isolated elevation in bilirubin
Gilbert’s syndrome
mild elevation of just bilirubin
2 or 2.5 (normal 1 )
hereditary un-conjugated bilirubin that is relatively common
acute pancreatitis
inflammatory condition that causes inflammation of the pancreas usually due to
choledocholitahiasis
ETOH abuse
alcohol pt with abd pain
pancreatitis!
Pancreatic enzymes released into circulation causes
a. Hypotension
b. ARDS
c. Disturbance of coagulation cascade
d. Hypocalcemia
go into shock
predominant symptom of acute and chronic pancreatitis
PAIN
epigastric sharp stabbing through and through doesn't wrap around (biliary tract) BORING --> hot poker
pancreatitis is exacerbated by
Eating (PUD better w/eating)
ETOH
vomitting
turns out enzymes for digestion and hurts
physical exam findings with pancreatitis
" Abdominal rigidity " Voluntary guarding " Fever " Tachycardia " Shock
pancreatitis dx test
” Abdominal pain film
“ CT abdomen is BEST
common lab finding specific to pancreatitis
increase amylase & lipase
other than increase in amylase what other labs diagnostics do we see
Hypocalcemia from release of pancreatic enzymes
Leukocytosis - elevation of WBC b/c inflammation present
BUN (b/c dehydration since they stopped eating or ARF)
Hyperglycemia b/c pancreas not working
LFTs (biliary obstruction pattern - Alk phos elevated)
biliary obstruction pattern
predominantly alk phos
Outcome of pancreatitis is influenced by -
a. Etiology: alcoholic doesn’t do as well
b. Co-morbidity: if they have hepatitis or HF not looking good
c. # of previous attacks:
in chronic pt who continues to drink alcohol
d. Severity of disease
complications of pancreatitis
- Prolonged hospitalization
- Shock
- Hypoxia - pleural effusions, respiratory distress
- GI bleeding - pretty common
- 25% develop pseudocysts - need sx
- Pancreatic abscess - need sx
Chronic Pancreatitis why do we see only slightly elevated amylases
not a lot of pancrease function left
can get just a mildly elevated amylase
need to go back to the history and see how much they are drinking and if they have ever had this before
clincal findings in chronic pancreatitis
Similar presentation to acute
ETOH pt’s may develop pancreatic insufficiency
30% have steatorrhea due to chronic calcific pancreatitis and malabsorption (floaty, oily, greasy stools)
GI bleeding and pancreatic hemorrhage common
Malabsorption seen with chronic pancreatitis
emaciation, peripheral edema, multiple
low total protein–> edema
bloated asceitis type belly
why would we see DM with chronic pancreatitis
Diabetes from endocrine insufficiency
jaundice with pancreatitis suggests
Jaundice suggests common bile obstruction
prognosis of chornic pancreatitis
Chronic pancreatitis as a primary cause of death is rare
Usually a consequence of associated complications -
management of chronic pancreatitis
a. ETOH abstinence!
b. Smaller, more frequent meals to reduce post prandial pancreatic secretions
c. Analgesics
d. Pancreatic enzymes w/ meals to reduce exogenous enzymes release
e. Restriction of dietary fat intake
complications of chronic pancreatitis
GI bleed Biliary tract infection Liver failure Malabsorption Electrolyte abnormalities
what are cholesterol stones made of
80-90% cholesterol
10% pigmented bilirubin
pigmented bilirubin stones are more common in
alcohol
only 10-20%
which percent of the population has gallstones
which % is symptomatic
10% of US population has gallstones
50% of these will be symptomatic
Cholelithiasis is most common with
4 F’s = Fat, Forty, Female, Fertile
CM of biliary colic
”
RUQ to mid-epigastric pain
Colicy pain –> intermittent
“
Sharp, maybe severe
Radiates to back/R shoulder. wraps around
Classically follows ingestion of fatty meal (1-2 hrs after meal)
PE with cholelithiasis
RUQ tenderness
(-)Murphy’s sign
inspiration cessation and pain
Dx
Based on hx, PE, normal labs, abdominal US
Polyp doesn’t have an acoustic shadow but a stone does on US
labs with biliary colic
amylase/lipase (pancreatitis)
CBC-infection or inflammation
cholecystitis you see elevation
cholelitahisis you should have normal cbc and normal liver test
maybeee elevation of alk phos
dx for cholelithiasis
RUQ abd ULS
management of biliary colic
need to have gallbladder out
cholecystectomy
NON surgical:
non surgical mngmt of cholelithiasis
- Non-surgical tx; 50% recurrence rate
a. Oral bile salts slowly dissolves stones
b. Lithotripsy
c. ERCP –> scope down to the gallbladder; if small enough and one stone, then can grab it and take it out
i. Not commonly done anymore
Prognosis for cholelithiasis
- Prognosis unrelated to severity of symptoms
- Complications increase with length of time symptoms are present
- Morbidity in pts who don’t have cholecystectomy
- If they don’t elect for sx then tell them to watch out for severe RUQ pain that doesn’t go away
Morbidity in cholelithiasis pts who don’t have cholecystectomy
a. Acute cholecystitis
b. Cholangitis with liver abscess
c. Necrotizing pancreatitis
d. Gallstone ileus with SBO
e. Gallbladder CA
CM of Acute Cholecystitis
" Severe, constant abd pain " Often epigastric, localizing to RUQ " Radiation to back, R shoulder " Exacerbation 1-2 hrs after meal " Fever
acute cholecystitis is usually caused by
inflammation of the gallbladder from obstructing stone
PE with acute cholecystitis
” Fever
“ RUQ tenderness
“ Involuntary guarding
“ (+) Murphy’s sign
differentiating cholecystitis from cholelithiasis
SEVERE CONSTANT PAIN
N/V/F
acute cholangitis
ascending infection of the biliary tract
results from acute cholecystitis
iii. Charcot’s Triad
acute cholangitis
” RUQ pain
“ Shaking chills & Fever
“ Jaundice
surgical emergency gall bladder out RIGHT NOW
Acute Cholecystitis lab
" Leukocytosis " Elevated Amylase, mild " Elevated ALT/AST, mild " Total bilirubin and Alk Phos typically not elevated " Order US
Acute Cholangitis labs
Leukocytosis w/ left shift (immature cell indicative of bacterial infection)
Elevated Alk Phos, Total (direct) bili, GGT
Variable elevations in ALT, AST
leukocytosis left shift is indicative of
bacterial infection
diagnostic test of cholecystitis
US of RUQ w/ acute cholecystitis –> marked thickening of gallbladder wall w/ fluid surrounding the distended gallbladder
mangmt of cholecystitis
- Admission
- IV empiric abx for gram negatives
- Pain management
- NPO, NG tube
- cholecystectomy
NPO, NG tube used for cholecystitis because
Want the gallbladder to rest since gallbladder most active when we are eating (it squirts a bunch of enzymes to digest the food)
Cholecystectomy definitive treatment because….
a. 30-40% will progress to gangrenous cholecystitis and perforation without surgery
vi. Treatment of acute cholecystitis vs acute cholangitis
1Don’t need to know details
Can wait a day or 2 depending on how busy the OR is, etc
Ascending cholangitis = they need emergency sx right now
Primary Sclerosing Cholangitis is usually associated with this dz and seen with abnormal liver function
Associated w/ inflammatory bowel disease
c. Primary Sclerosing Cholangitis
inflammation and fibrosis in the biliary tree need to screen for it because
complications of primary sclerosing cholangitis
Primary Biliary cholangitis (primary biliary cirrhosis)
ii. Recurrent pyogenic cholangitis
iii. Cholangiocarcinoma
Rare bile duct cancer, often associated with PSC, presenting with painless jaundice, right upper quadrant abdominal pain, and weight loss
Cholangiocarcinoma
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
Recurrent pyogenic cholangitis
Rare T-lymphocyte-mediated attack on small intralobular bile ducts; affects women (95%) age 30-65
Primary Biliary cholangitis (primary biliary cirrhosis)
An obese 37-year-old female is in the emergency room for right-sided abdominal pain and excessive flatulence. This episode has persisted for several hours. On physical exam you palpate her right upper quadrant while she takes a deep breath. The patient experiences pain and has a transient pause in inspiration. What is the most likely diagnosis?
acute cholecystitis
+Murphy’s sign makes acute cholecystitis most likely; biliary colic may present with similar symptoms but will not have +Murphy’s sign
A 50-year-old woman presents to the clinic with a two-day history of right upper quadrant pain. She has a history of hypercholesterolemia and her examination is significant for a positive Murphy’s sign. What is the preferred imaging modality?
abdominal ultrasound
A 72-year-old man presents with concerns of “looking yellow.” He is asymptomatic but admits to an unintentional 15 pound weight loss over the last two months. Physical examination reveals jaundice, mild epigastric tenderness, and palpable periumbilical nodules. Which of the following is the most likely diagnosis?
pancreatic cancer
A 43-year-old woman presents with episodic epigastric pain that frequently follows a fatty meal and can last anywhere from 15 minutes to approximately two hours. At times the pain radiates toward her right shoulder. She has associated nausea without vomiting. Which of the following is the most appropriate next step in managing this patient?
US of the abdomen
A 57 y/o male has routine lab work for a physical exam; he is generally healthy and asymptomatic. His fasting labs reveal an elevated Alk Phos; the remainder of his CMP is normal, as is his CBC. What is the next step in the evaluation of this abnormal result?
order serum GGT and alkaline phosphatase isoenzyme
A 63 y/o male c/o abdominal pain x 1 week with anorexia, no weight loss or vomiting, no jaundice. Labs reveal AST 250 (normal 10-40), ALT 150 (normal 10-40), Alk Phos 185 (normal 40-150); amylase and lipase are both mildly elevated. Which of these is the most likely etiology of these abnormal lab results?
alcohol use
normal alk phos
44-147
why would you see an increase in bilirubin and ALP in a pt with chronic pancreatitis
secondary to extra hepatic biliary obstruction
crampy
sharp
RUQ
cholecystitis
usually follows fatty meal
charcot’s triad
for acute cholagitis
fever chills
RUQ pain
jaundice
reynold’s triad
fever chills
RUQ pain
jaundice
(carchot’s )
shock and altered mental status acute cholangitis
