Biliary Diseases Flashcards
what are the liver function tests?
ALT, AST, Alkaline Phosphatase, GGT, LDH, Bilirubin
what is ALT? found where? released when? normal range?
type of LFT
found primarily in hepatocytes
released when cells are hurt or destroyed
normal is b/w 7-55 U/L
when does ALT increase?
whenever the hepatocytes are injured
do the LFTs test the function of the liver?
NO!!! they are just enzymes that are created in the liver
what is AST? found where?
type of LFT
Found in liver, heart, muscle, intestine, pancreas
is the AST specific for liver disease?
no!!! when it goes up, doesn’t always mean the liver or hepatocytes are damaged - could be something else
what does the AST follow?
the ALT - when ALT increases, so does AST
when is AST elevated 2 or 3x (vs ALT) giving an AST/ALT ratio >3?
Elevated 2 or 3x (vs ALT) in alcoholics
AST/ALT ratio >3 = alcohol underlying cause
AST normal range
8-48 U/L
what is alkaline phosphatase? found where?
type of LFT
found in liver (esp biliary tract), bones, intestines, & placenta
when does the liver alkaline phosphatase rise? GGT?
with obstruction or infiltrative diseases (i.e. gallstone or tumors)
GGT is considered more specific to liver than AP (helps you determine if AP is elevated d/t biliary disease)
what is the normal range of alkaline phosphatase?
45-114 U/L
what is GGT?
enzyme found in many organs - highest concentration in the liver
a type of lLFT
when is GGT elevated?
elevated in blood in most diseases that cause damage to liver or bile ducts
the first enzyme to be elevated in damage to the liver
if alk phos is elevated and unsure if d/t bone or liver, what do you check?
the GGT
if normal GGT then likely d/t bone disease
if GGT elevated in setting of Alk phos, d/t liver disease
(elevated in 75% of ETOH abuse)
what is LDH? elevated in? found where?
type of LFT
enzyme found in blood and liver
elevated in tissue damage, so if liver damaged, may be elevated
what is bilirubin?
yellow pigment formed in the liver by the breakdown of Hgb and excreted in bile
when is bilirubin elevated?
- jaundice
- liver disease and blockage of the bile ducts
- any process which increases the breakdown of RBCs (hemolytic anemia)
- anything that affect the production or elimination of bilirubin
what are the 2 forms of bilirubin?
unconjugated bilirubin “indirect”
conjugated bilirubin “direct”
what is unconjugated bilirubin “indirect”?
heme that is released from Hgb is converted to unconjugated bilirubin
it is carried by proteins to the liver
small amounts may be present in the blood
what is conjugated bilirubin “direct”?
when unconjugated bilirubin gets sugars added to it in the liver
it enters the bile and passes from the liver to the small intestines and is eliminated in the stool
normally, no conjugated bilirubin is present in the blood
total bilirubin range?
0.3 - 1.9 mg/dL
conjugated + unconjugated
normal range of bilirubin?
0-0.3mg/dL
hepatocellular pattern of liver enzymes
increased AST and ALT compared to Alk phos, bili +/- elevated
Ex: intrahepatic injuries
Hepatocytes damaged -> ALT and AST released from cells
cholestatis pattern of liver enzymes
increase in alk phos compared to AST, ALT, bili +/- elevated
elevated in biliary obstruction or duct injury d/t retention of bile acids in the liver
Extrahepatic - ex. biliary obstruction
Intrahepatic - ex. primary biliary cholangitis
isolated hyperbilirubinemia pattern of liver enzymes
increase in bilirubin but the AST/ALT and alk phos are normal
what are the 3 sections of the gallbladder?
fundus, body, neck
what is the common bile duct?
cystic duct + hepatic duct join
what is the fxn of the gallbladder?
- stores bile
- bile emulsifies fats - assisting in absorption of fats
what is bile?
bile acids + phospholipids + cholesterol
what is the function of bile?
used to help excrete cholesterol, aid in the digestion and absorption of fat, cholesterol and fat soluble vitamins in the intestines (A, D, E, K)
where are bile acids stored?
in the gallbladder
where are bile acids reabsorbed?
in the terminal ileum and then carried through the portal blood circulation to be reconjugated and secreted back into the bile
what is cholestasis?
something is obstructing the secretion of bile
causes of cholestasis?
- gallstones
- gallstones in common bile duct
- tumors
- cysts
- pancreatic problems
- liver disease
cholestasis s/sx’s
RUQ pain, colicky, jaundiced, dark urine, weight loss
what liver enzyme will be elevated in cholestasis?
alk phos will be elevated
dx of choelstasis
US to look for stones, tumor or cause of blockage
CT or MRI (liver disease)
-MRI better for looking at liver, but can do CT if uncertain
what is cholelithiasis?
gallstones
pathophysiology of cholelithiasis?
-form secondary to abnormal bile constituents
mechanism of gallstone formation:
- increased biliary secretion of cholesterol
- cholesterol crystals precipitate and form stone
- gallbladder hypomotility
what are the 2 types of gallstones and which one is most common?
cholesterol stones (MOST COMMON)
pigment (calcium) stones
cholelithiasis epidemiology
women > men
increases with age
native Americans
cholelithiasis risk factors
- **4 Fs
- Fat, Fertile, Forty, Fair
- obesity, pregnancy/OCP, age, fair skin
-forty is the magic number - incidence 4x higher b/w ages 40-69
cholelithiasis clinical presentation
-MANY ARE ASYMPTOMATIC (until stone gets stuck)
- intermittent severe RUQ pain radiation to the scapular region (d/t diaphragm innervation)
- pain can be epigastric w/radiation to the RUQ
-onset is sudden and can last from 30min - 5 hrs
- N/V w/pain
- pain can occur after eating high-fat meal
- night>day
cholelithiasis dx
US - very sensitive even for small stones
-can use the US to assess the emptying and filling of the gallbladder
Plain film - won’t see many cholesterol stones (see pigment stones)
HIDA - looks at the functioning and emptying of the gallbladder
-determines if a cystic duct obstruction is present
what does the HIDA scan do?
looks at the functioning and emptying of the gallbladder
-determines if a cystic duct obstruction is present
used in cholelithiasis dx
US may not show obstruction so use HIDA scan
when do you treat cholelithiasis?
only if pt is symptomatic
tx of cholelithiasis
laparoscopic cholecystectomy for symptomatic patient
-outpatient, w/ quick recovery, not for urgent/emergent
chenodeoxycholic and ursodeoxycholic acid if pt is symptomatic
- requires lifelong administration
- bile salt given PO to dissolve stones over 2 years time
- for pts who refuse surgery and have a functioning gallbladder
- gallstones do recur
who is chenodeoxycholic and ursodeoxycholic for?
its for tx of cholelithiasis if pt is symptomatic
-for pts who refuse surgery and have a functioning gallbladder
acute cholecystitis caused by?
gallstone obstruction (most of the time) -gallstones obstruct the cystic duct
acute cholecystitis sx’s? PE signs?
RUQ/epigastric pain that is continuous and gradually worsens
fever, leukocytosis, N/V, anorexia
PE signs:
+ Murphy’s sign (pain on inspiration while press on RUQ)
-Courvoiser’s sign: a palpable gallbladder on PE b/c gallbladder dilates d/t obstruction of common bile duct
what is acalculus cholecystitis?
an acute inflammatory condition in pts w/out gallstones
acute cholecystitis labs
***elevated WBC (b/c of infection) - (leukocytosis with left shift)
-increased bili, increased AST/ALT
acute cholecystitis imaging
RUQ US - shows stone and inflammation but not obstruction
Sonographic Murphy’s sign (+ Murphy’s sign when press US into RUQ)
HIDA scan - shows cystic duct obstruction
acute cholecystitis tx
NPO, IVF, Pain control (caution with Morphine)
IV abx (3rd gen cephs + Flagyl; severe cases need Fluoroquinolone + Flagyl)
LAP CHOLECYSTECTOMY - MAINSTAY
why must you be cautious with Morphine when treating the pain of acute cholecystitis?
b/c Morphine can cause spasm of the sphincter of Oddi
what is the mainstay of tx for acute cholecystitis?
lap cholecystectomy
often done w/in first 24-48 hrs after presentation or, less often, 4-8 wks after an acute episode
tx for acute cholecystitis pts that aren’t surgical candidates
percutaneous drainage
-relieves pressure in gallbladder
what is choledocolithiasis?
stone that gets into the common bile duct
-can form spontaneously in the duct even after cholecystectomy
COMPLICATION OF CHOLELITHIASIS
choledocolithiasis labs
very elevated ALT/AST from obstruction, often >1000
elevated bilirubin
alk phos will rise slowly
choledocolithiasis imaging
RUQ US and CT will show dilated ducts from stuck stone causing inflammation
MRCP (special type of MRI)
ERCP - reserved for therapeutic interventions - do sphincterotomy w/stent placement (take out stone and put in stent)
what is cholangitis?
inflammation of the bile duct, complication of choledocolithiasis
cholangitis s/sx’s
CHARCOT’S TRIAD - fever, jaundice, severe RUQ pain
pruritis (b/c elevated bilirubin), dark urine, alcoholic stools
REYNOLDS PENTAD = Charcot’s triad + Hypotension and AMS
***THESE PTS ARE SICK, ENDOSCOPIC EMERGENCY
what is Charcot’s triad?
fever, jaundice, severe RUQ pain
indicative of cholangitis
what is Reynolds pentad?
Charcot’s triad (severe RUQ pain, fever, jaundice) + hypotension and AMS
is cholangitis an emergency?
YES!!! ***THESE PTS ARE SICK, ENDOSCOPIC EMERGENCY
cholangitis tx
Hang IV abx and go to ERCP stat (endoscopic sphincterotomy and stone extraction is key!!!)
-Ampicillin + Gentamycin or Cipro + Flagyl
After pt stable and stone is out, then do lap cholecystectomy
what is key for cholangitis tx?
Endoscopic sphincterotomy and stone extraction
once cholangitis pt is stable, how are they treated?
lap cholecystectomy
what is primary sclerosis cholangitis?
chronic diffuse inflammation of the biliary system
leads to fibrosis and stricture of the biliary ducts
very rare
primary sclerosis cholangitis risk factors
- ***UC
- Crohn’s, 1st degree family member, HLA-88, DR-3, DR-4
primary sclerosis cholangitis epidemiology
Men > women
age 20-50
primary sclerosis cholangitis clinical presentation
- progressive obstructive jaundice
- fatigue
- pruritis
- anorexia
- indigestion
primary sclerosis cholangitis labs
elevated alk phos
low serum albumin (d/t malabsorption)
primary sclerosis cholangitis dx
ERCP, MRI
Liver Bx - periductal fibrosis “onion skinning” - histology and antibody studies to look for autoimmune disease
primary sclerosis cholangitis complications
-cholangocarcinoma (Cancer of the common bile duct - very poor prognosis)
- gallstones
- cholecystitis
- gallbladder polyps
- gallbladder carcinoma
primary sclerosis cholangitis tx for acute bacterial
cipro 750mg BID - high dose
chronic primary sclerosis cholangitis tx
Balloon dilatation or stenting (keeps duct open)
resection of dominant stricture
UC pts - colorectal screening to reduce colon cancer
cirrhosis + primary sclerosis cholangitis -> need liver transplant
cirrhosis + primary sclerosis cholangitis pts need what tx?
liver transplant
what type of organ is the pancreas?
retroperitoneal
what does the sphincter of oddi do?
smooth muscle sphincter present around the common channel of the pancreatic duct and common bile duct
prevents reflux of duodenal juices into the pancreatic duct and CBD
function of the pancreas?
part of the endocrine and digestive system
make endocrine hormones - insulin, glucagon, somatostatin
digestive - assists in digestion and absorption of nutrients in the small intestine; helps breakdown carbs, proteins, lipids
what is the pathogenesis of pancreatitis?
not well understood
may include edema or obstruction of the ampulla of Vater or reflux of bile into pancreatic duct
(bile that is supposed to dump into small intestines is backed up and goes back into pancreatic duct)
acute pancreatitis
occurs suddenly and may result in life-threatening complications
interstitial vs necrotic, 80% recover
recurrent pancreatitis
25% will have a recurrence
most often d/t alcohol or cholelithiasis
acute pancreatitis most common what?
most common inpatient GI dx
most common causes of acute pancreatitis?
gallstone and chronic alcohol abuse account for 2/3 or more cases in US
older age = what for acute pancreatitis?
worse prognosis
what are the 2 most common occurrences of acute pancreatitis?
interstitial pancreatitis occurs most commonly
-acute inflammation of the pancreas and peri-pancreatic tissues W/OUT TISSUE NECROSIS
necrotizing pancreatitis
-inflammation associated w/pancreatic parenchymal necrosis and or peri-pancreatic necrosis and PANCREATIC BLOOD SUPPLY IS INTERRUPTED
2 most common causes of acute pancreatitis?
GALLSTONES - MOST COMMON!!!
Alcohol
acute pancreatitis complications
Multisystem Organ Failure - 30% mortality, after 48hrs increases to 50%
Ileus - large & small intestines stop moving
Pseudocyst - low incidence
Pancreatic necrosis - 17% mortality risk, may need percutaneous aspiration, abx, debridement
-pancreas starts digesting itself
what are s/sx’s of Multisystem Organ Failure for acute pancreatitis?
Renal Failure - pre renal azotemia, may require dialysis in severe cases
Acute Respiratory Distress Syndrome - fluid not from cariogenic source, intravascular leakage of fluids in pancreatic bed and lungs
acute pancreatitis sx’s
mid epigastric pain - abrupt onset, relieved with sitting forward -> HALLMARK
- pain radiates to back
- N/V are common
what is the hallmark sx of acute pancreatitis?
mid epigastric pain - abrupt onset, relieved with sitting forward
acute pancreatitis signs
- EPIGASTRIC TENDERNESS
- jaundice, nausea
signs of severe pancreatitis
Tachypnea, hypoxemia, hypotension
Cullen’s Sign (retroperitoneal hemorrhage around the umbilicus - bruising)
Grey Turner’s sign (ecchymosis of the flanks)
acute pancreatitis hx work-up
- gallstones
- alcohol use
- hypertriglyceridemia
- autoimmune diseases affecting the pancreas
- fam hx of pancreatic d/o
- med hx
acute pancreatitis lab analysis
Amylase - 3x ULN (elevated, but short half-life so falls w/acute episode so less sensitive)
LIPASE - 3x ULN
acute pancreatitis imaging
CT scan of Abdomen IV contrast
Abd US
MRI
NOT NEEDED FOR DX
is acute pancreatitis imaging needed for dx?
NO!!!
CT scan is saved usually saved for when deteriorating
pancreatitis dx ≥2 of the following…
≥2 of the following:
- characteristic midepigastric and pain +/- radiation to the back
- lipase and/or amylase 3x ULN
- CT confirmation of pancreatitis (don’t need this)
acute pancreatitis management
- admit to hospital (b/c decompensate quickly)
- find and treat underlying cause
- **-NPO (give pancreas a rest)
- IVF (Lactated Ringer’s or NS)
- analgesia
- repeat labs assessing BUN/Cr, HCT q8-12 hrs
how often do you repeat labs for acute pancreatitis and why?
repeat labs of BUN/Cr, HCT q8-12 hrs
helps determine how severe and how quickly they are going to deteriorate
want to make sure fluid won’t go into their lungs
acute pancreatitis severity predictor scores
Ranson criteria (most common)
Apache II score
SIRS (systemic inflammatory response syndrome) score
BISAP
what is the Ranson criteria?
Estimates mortality from pancreatitis. Done on admission (5 tests) and after 48h (6 tests). Poor predictor but used often.
scores of Ranson criteria for acute pancreatitis
1-3 = mild pancreatitis
> 3 = more severe pancreatitis
what is the SIRS score?
Predict severity of pancreatitis. Easily done at bedside. Temp, HR, RR, WBC.
reliably predicts severity of pancreatitis
tells you if pt is systemically sick
difference b/w Ranson criteria and Apache II score?
Apache II score can be performed daily
what is mild acute pancreatitis?
w/out local complications or organ failure
self-limited, subsides in 3-7 days
what is moderate severe acute pancreatitis?
- transient organ failure (<48 hrs)
- local systemic complications minus organ failure
- may/may not develop a local complication such as pseudocyst
what is severe acute pancreatitis?
persistent organ failure >48 hrs
CT scan to assess for necrosis recommended
what is chronic pancreatitis?
irreversible damage to the pancreas as distinct from the reversible changes noted in acute pancreatitis
histologic abnormalities, including chronic inflammation, fibrosis, and progressive destruction of both exocrine and eventually endocrine tissue (atrophy)
-can be inflammatory response to its own hormones & digestive enzymes
what is the most common cause of chronic pancreatitis?
alcohol abuse
causes of chronic pancreatitis
- ALCOHOL ABUSE (M/C)
- Idiopathic
- Cig smoking (esp if alcoholic)
- cystic fibrosis (children)
- genetic defects
- autoimmune pancreatitis
chronic pancreatitis complications
- NARCOTIC ADDICTION (b/c of so much pain)
- Diabetes/impaired glucose tolerance - b/c pancreas makes insulin and now can’t make it
- gastroparesis (intestines stop working)
- malabsorption
- biliary stricture
- pancreatic carcinoma - hereditary pancreatitis 10x incr risk of pancreatic cancer
chronic pancreatitis sx’s
calcifications, steatorrhea, and DM - classic
-abd pain, anorexia, N/V, weight loss
chronic pancreatitis signs
PE findings are unimpressive
tenderness over pancreas - during attacks
chronic pancreatitis dx (labs and imaging)
NO BIOMARKER FOR DISEASE SO HARD TO DX
Labs:
- amylase/lipase mild-normal elevation
- glucose may be elevated
- secretin test: abnormal when >60% of pancreatic exocrine fxn has been lost (takes long time to occur)
Imaging:
abd CT is initial modality of choice
-not done every time pt has exacerbation, just for dx
chronic pancreatitis tx
Low fat diet, no EtOH.
Abd pain=Hard to treat, try TCAs. Avoid opiates.
Steatorrhea=pancreatic enzyme
Endoscopic tx - sphincterotomy, stenting, stone extraction, drainage of pseudocyst
Whipple -> usually for tumor in head of pancreas
what is diverticulosis?
a weakness in the wall of the colon resulting in outpouching (diverticula)
-mucosa and submucosa herniate thru muscle layer
-dx with colonoscopy
what is diverticular bleed?
painless bleeding of diverticula
diverticula have blood supply -> so can bleed
what is diverticulitis?
inflammation of diverticulum
EXTREME PAIN
diverticulosis most common in what age? most common where in the colon? strongly correlated with what?
- M/C in ppl >80 y/o
- M/C is sigmoid diverticulosis (left side)
- westernized diet strongly correlated
complications of diverticula
they can perf and the contents are now in the peritoneal space
diverticulosis risk factors
- age
- constipation (puts pressure on colon and causes weakness -> diverticula)
- diet (high fat and red meat)
- obesity
- genetics (connective tissue disorders)
- physical inactivity
Complication of diverticulitis
- abscess
- obstruction
- perforation
- fistula (protrusion connects to bladder -> contents of the diverticula go into the bladder)
diverticulosis dx
COLONOSCOPY
other studies incidental finding:
-CT, MRI, Barium Enema
recurrent complications of diverticulitis
chronic abd pain; fibrosis w/strictures lead to ileum and bowel obstructions
diverticulitis sx’s
Abd pain in LLQ that is CONSTANT AND LASTS SEVERAL DAYS (not colicky pain - doesn’t start/stop abruptly)
N/V, fever
Change in bowel habits
(constipation b/c of inflammation; diarrhea b/c body trying to rid infection)
diverticulitis signs
Abd tenderness in LLQ - guarding, rigidity, rebound
diverticulitis PE
vital signs, heart and lungs, abdomen, pelvis (female), back
diverticulitis work-up labs
CBC w/diff
BMP - electrolytes can be off w/diarrhea
Urinalysis - looking for translocation of bacteria into the bladder
diverticulitis work-up imaging
ABD CT/PELVIS WITH IV CONTRAST +/- PO CONTRAST
-hard for pt to swallow so do IV if can’t do PO
Abd and CXR - good for ileum, pneumoperitoneum (free air)
Can also do KUB - kidney urinary bladder Xray to see if any perforations
diverticulitis management options - medical vs complicated
If complicated - ADMIT
Medical: acute uncomplicated can be treated non-operatively
Acute Complicated:
- Micro perf = medical management
- Abscess = may require IR drainage
- Free perf = EMERGENCY SURGERY
- Significant obstruction = Urgent to Emergent surgery
acute diverticulitis medical management
Antibiotics - cover for enterobacteriaciae & gram neg anaerobe (B. Frag)
-Cipro & Flagyl
IVF (admitted)
Analgesia & antiemetics PRN (IV vs PO)
NPO vs Clear Diet vs normal diet
acute diverticulitis goal of surgical management
to restore intestinal continuity if possible
when do you do emergent surgery for diverticulitis?
free perf, +/- bowel obstruction
when do you do urgent surgery for diverticulitis?
failure of medical tx; colonic obstruction; abscess failing non-operative intervention
when do you do elective surgery for diverticulitis?
persistent pain, fistula development, pt w/prior diverticulitis complication, immunocompromised pt w/prior acute diverticulitis
diverticulitis surgery options
One-Stage Procedure
-colon resection w/primary anastomosis (cut out diverticula and anastomose)
Two-Stage Procedure
- colonic resection w/end colostomy (Hartmann’s procedure)
- primary anastomosis w/diverting ileostomy
what criteria do surgeons use to determine which procedure (One or Two stage) for diverticulitis?
Hinchey Classification Systems
diverticulitis follow-up
Colonoscopy - for NEW DX of diverticulitis
- do 6 weeks post-infection unless had one in last year (NEVER IN SOMEONE W/ACTIVE DIVERTICULITIS)
- r/o colon cancer
- assess diverticular disease
Diet Modifications
-consumer high fiber diet or long-term fiber supplementation
Diverticular bleeding epidemiology
- hemorrhage occurs in 5% w/diverticulosis
- M/C cause of overt (hematochezia or maroon) lower GI bleeding in adults
- MOST STOP SPONTANEOUSLY
Diverticular bleeding etiology
vasa recta recurrent injury leading to weakness and bleeding
RIGHT COLONIC DIVERTICULA = MAJOR SOURCE
Diverticular bleeding sx’s
PAINLESS hematochezia
PAINLESS maroon-color mixed w/stool (blood mixed with stool)
Bloating, cramping, urge to defecate (blood increases urge)
Hemodynamically unstable: syncope, lightheadedness, postural dizziness
Diverticular bleeding signs
Abd - benign
BRBPR or dark
hemodynamically unstable
hypotension, tachycardia, pallor
diverticular bleeding dx lab
Hgb/Hct - normal to decreased (MCV normal)
BMP - BUN/Cr normal
Diverticular bleeding dx imaging
COLONOSCOPY - when pt is stable
Nuclear scintigraphy (tagged RBCs to see where bleeding from)
Angiography
Diverticular bleeding PE
Vital signs: stable or unstable
Eyes/mouth: pale conjunctiva
Heart: tacky
Abdomen: soft, non-tender, active bowel sounds
Rectal: gross blood present
Anoscopy: no hemorrhoids (make sure no hemorrhoids b/c they love to bleed)
Diverticular bleeding management
Resuscitation
- two large bore IVs - need to put in fluid quickly
- IVF NS
- Type and Cross for blood - if Hct is dropping
- Transfuse PRBCS pro
+/- NGT to r/o UGI
-if blood is dark and difficult to differentiate melena
Intervention if needed:
-bleeding often self-limited
Diverticular bleeding surgery
COLONOSCOPY
-treat active bleeding w/submucosal epinephrine or endoscopic tamponade (makes blood vessels constrict and stop bleeding)
Angiography - alternative to colonoscopy, infuse vasoconstrictors
when do you do surgery for Diverticular bleeding?
- hemodynamically unstable
- endoscopic or angiographic therapy unsuccessful
- pts w/ recurrent episodes of bleeding
what pts are more likely to get gallstones?
pts w/sickle cell anemia are more likely to get gallstones b/c have chronically elevated bile
what is Courvoiser’s sign?
seen in acute cholecystitis
a palpable gallbladder on PE b/c gallbladder dilates d/t obstruction of common bile duct
when is unconjugated bilirubin found in urine?
only with renal disease
