GI: Biliary + Hepatic Flashcards
Cholelithiasis
- list the type of stones and causes
- RF
- CM
- Diag–TOC
gallstones in biliary tract (in GB)
- Cholesterol stones yellow to green
- obesity
- DM
- hyperlipidemia
- OCPs
- Native americans
- cirrhosis
- CF
- CD - Pigmented stones
* black stones: assoc with hemolysis or ETOH cirrhosis
* brown stones: assoc with biliary tract infection - mixed stones—MC*****
- components of both cholesterol and pigment stones
RF: fat, fertile, female, forty, fair *OCP use *native americans *bile stasis *chronic hemolysis *corrhosis *infection *rapid wt loss *IBD *fibrates
CM
*most asympto
+biliary colic—HALLMARK–episodic, abrupt RUQ or epigastric pain
*sometimes occurs after eating at night–esp fatty foods
*can last 30 mins to hours
Diganosis:
- RUQ US–initial TOC
- CT scan or MRI are altneratives
TX:
- asympto– no tx
- sympto: cholecystectomy if recurrent s/s
Cholecystitis *etiologies CM PE diagnosis--TOC, most accurate test, labs
Etiology:
- MC caused by gallstone lodged in cystic duct–causes inflammation of GB
- 10% of PTs with gallstones
- E. coli commonly implicated
CM:
*pain is similar to cholelithiasis
+continuous (gallstones is colic) RUQ pain (dull, achy)–precipitated by fatty foods or large meals
+/- nausea, vomiting, guarding anorexia
PE: \+enlarged, palpable GB \+fever--low grade \+Murphy's sign--pathognomonic \+Boas sign: reff pain to the right shoulder or subscapular area--- due to phrenic nerve invervation
Diagnosis:
TOC: RUQ sonogram–thickend or distended GB
*if US inconclusive.. most accurate test=HIDA scan..+ if cannot see GB
LABS: incr WBCs, incr billirubin, incr alkaline phosphatase and incr LFTs
TX:
- admit and NPO
- IV hydration, pain meds, electrolytes
- IV ABX: Ceftriazone covers gram- & Metronidazole covering anaerobics
- cholecystectomy w/in 72 hours
- recurrance rate with nonsurgical tx is very high– almost 70%—why we counsel PTs to do surgery!
Choldedocholithiasis
CM
diagnosis–labs, initial image of choice, gold standard
gallstone in common bile duct
CM -prolonged biliary colic RUQ \+nausea \+vomiting -jaundice******
Diagnosis:
LABS: elevated AST & ALT, incr alkaline phosphatase
*RUQ US=initial image of choice–not sensitive and only detects 1/2 the cases—-so cannot be used to r/o
*ERPC–gold standard–diagnostic + therapeutic
TX:
*ERCP with stone extraction
Acute Ascending Cholangitis
*etiologies
CM
Diagnosis: labs, initial TOC, most accurate, gold standard
Etiologies:
obstruction–>infection–>biliary stasis–>bac overgrowth
most infections due to E. coli*** or other gram- enteric organisms that ascend from duodenum
CM:
- Charcot’s traid: fever/chills + RUQ pain + jaundice
- Reynold’s pentad: Charcot’s triad + hypotention or shock + AMS
Diagnosis:
LABS: leukocytosis, incr alkaline phosph and incr Gamma-glutamyl transferase (GTT), incr bilirubin, midly incr ALT and AST
RUQ US: intial TOC
MRCP: most accurate TOC
GOld standard: Cholangiography with ERCP–usually not done until PT is stable and afebrile for 48 hours after ABX
Initial Management:
- IV ABX followed by CBD decompression & stone extraction once stable
- ABX= Ampicillin/Sulbactam, Piperacillin/tazobactam, Ceftriaxone + metronidazole, fluroroquinolone + metronidazole, ampicillin + gentamycin
* anything to cover gram neg and anaerobes** - ERCP:
- PTC–drainage with catheter
- open surgical decompression and T-tube insertion for drainage
- Eventually, PT should undergo elective cholycstectomy
Primary Biliary Cholangitis/Cirrhosis (PBC) -define -what kind of dz -MC in? -CM PE -diagnosis.. hallmark? definitive? tx-first ? curative?
chronic and progressive cholestatic liver dz
*destruction of intrahepatic/lobular bile ducts with portal inflammation and scarring– leads to decreased bile salt excretion
- autoimmune dz**
- progresses to cirrhosis and end stage liver dz
MC in women 30-60 YO
CM
- asymptomatic
- fatigue
- pruritis (early)
- RUQ discomfort
- jaundice (later)
- osteoporosis
- portal HTN
PE:
- hepatomegaly
- jaundice
- xanthelsama
Diagnosis: \+ antimitochondrial antibodies (AMA) cholestatic LFTs= incr ALK-P and GGT Elevated cholesterol.. HDL Abd US to r/o biliary obstruction Liver biopsy--definitive
TX:
1st line: Ursodeoxycholic acid–can slow progression of the dz by preventing synthesis and absoprtion of cholesterol
2nd. Obeticholid acid
*for pruritis—cholestyramine and UV light
*vit D calcium to prev osteoporosis
Curative—liver transplant
Primary Sclerosing Cholangitis (PSC) -define -strongly associated with? -MC in who CM Diagnosis--most accurate test? hallmark finding?
chronic idiopathic progressive dz of intrahepatic and/or extrahepatic bile ducts characterized by thickening of bile duct walls and narrowing of the lumen
— leads to cirrrhosis, liver failure and cholangiocarcinoma
RF:
*UC very strongly related
MC in men 20-40 YO
+genetic predisposition
CM: *chronic cholestasis findings---- jaundice + pruritis \+fatigue \+RUQ pain \+hepato or splenomegaly
Diagnosis:
- cholestatic pattern–incr alk phosph and GGT,
- incr ALT AST, biri, IgM
- POSITIVE P-ANCA is hallmark ***
- most accurate test is MRCP, ERCP — see a beaded apperance of biliary tract
- liver biopsy not usually done
Management:
- stricture dilation for sympto tx
- cholestyramine for pruritis
- definitive= liver transplant
differences between PBC and PSC
PBC:
- intrahepatic, Anti-mitochondrial antibodies
- Intra and extra hepatic, hx of UC, and +PANCA
Cholangeocarcinoma
- define
- type of CA and MC in who
- assoc with
CA of biliary tree– this is not GB CA
adenocarcinoma in elderly MC
assoc with PSC and gallstones
CM: non specific and suggestion bile duct obstrction \+jaundice \+biliary colic \+wt loss -anorexia -RUQ mass
very bad prognosis– more than 90% die in 1 year
Nonalcoholic Fatty liver Dz
-etiologies
types
-diagnosis
etiologies:
- obesity
- hyperlipidemia
- long term steorid use
- DM
Types:
- Nonalcoholic fatty liver (NAFL)= relatively benign–NOT assoc with any malig
- Nonalcoholic steatohepatitis (NASH)=assoc with inflamm and fibrosis—can progress to cirrhosis—potentialy malignant
diagnosis:
- liver biopsy
TX:
-corrct underlying cause
acute hepatitis
- different phases
- lab work?
- prodromal phase–malaise, arthralgia, fatigue, URI s/s, anorexia, N/V, abdominal pain, loss of appetite, acholic stools
- icteric phase=jaundice
- Fulminant phase–acute hepatic failure–encephalopathy, coagulopathy, hepatomegaly, jaundice, edema, ascites, asterexis, hyperreflexia
labs: increased ALT and AST– may have hyperbilirubinemia
clincal recovery usually occurs w.in 3-16 weeks
causes of fulminant hepatitis (acute hepatic failure)
acetaminophen toxicity is MCC in the us
- viral hepatitis
- autoimmune hepatitis
- drug rxns
- sepsis “shock liver”
- Reye syndrome–in kids who are given aspirin during/after viral infection
CM for Fulminant Hepatits
- encephalopathy: coma, seizures, vomiting, asterixis
- coagulopathy (increased INR, PT and eventually incr PTT)
- hepatomegaly
- jaundice (NOT usually seen with reye)
reye syndrome
CM
RASH–hands and feet, intractable vomiting, liver damage, enephalopathy, dilated pupils with minmial resp to light and multiorgan failure
*kids who take ASA
diagnosis for fulminant hepatits
- clinical
- hypoglycemia: due to hepatic gluconeogenesis, incr ammonia (encephalopathy)
- labs: look at acetominophen levels, abnoral ALT, AST, coags, bilirubin,
Management for fulminant hepatitis
-definitive?
Supportive: IV fluids, electrolyte repletion
Mannitol if ICP elevation (elevated ammonia, direct toxin–>edema)
PPI stress ulcer prophylaxis
Platelets, FFP for coagulation factors if bleeding
Definitive is liver transplant
