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
Cirrhosis
- MCC
- other etiologies
CM
PE
management
complications
MCC is chronic Hep C and ETOH Etiologies: -acholic liver dz-->range of conditions from fatty liver to cirrhosis -chronic Hep B -Drugs-- tylenol, methotrexate -autoimmune hepatitis -primary biliary cirrhosis (PBC) -hemochromatosis -wilson's dz
CM
- fatigue
- weakness
- wt loss
- muscle cramps
- anorexia
- hepatic enchepalopathy: confusion and lethargy from increased ammonia levels (PE will show asterixis which is flapping tremor of wrists)
- esophageal varices
- jaundice +/- pruritis
PE
- ascites
- hepatosplenomegaly
- gynecomastia
- spider angioma
- telangiectasis
- caput medusa
- muscle wasitng
- bleeding
- palmar erythema
- jaundice
TX:
- avoid ETOH and hepatoxic drugs
- weight reduction
- vaccinations for Hep A and B to prevent additional insult
- tx underlying causes when possible
- liver transplant is definitive
Complications:
- end stage liver dz
- heptocellular carcinoma
- esoph varices
- spontaneous bacterial peritonitis
how to treat hepatic encephalopathy?
Lactulose ***
or
rifaximim
both first line
how to teat ascites
sodium restriction
diruetics (spironolactone, furosemide)
paracentesis
Pruritis with jaundice
Cholestyramine–bile acid sequestrant—reduces bile salts in skin–less irritation
what is the name of the surgery used to fix bleeding varices
TIPS–transjugular intrahepatic portosystemic shunt
**intervention of last resort– mortality rate is very high and it can lead to hepatic ecephalopathy with incr ammonia
Wilson Disease
CM:
Diagnosis
CM:
- liver dz
- CNS findings–dysarthria (MC), dystonia, Parkinson-like symptoms (bradykinseia, tremor, rigidity), dementia, ataxia
- Psych: depression, personality changes, psychosis and delusions
- kayser-Fleischer rings (cornea)
Diagnosis:
- Lab: decreased serum ceruloplasmin by 90%
- hepatic Dz findings: elevated transaminases, hemolytic anemia
- incr 24-hour copper excretion
- genetic testing for gene ATP7B
- Liver biopsy–definitve: if +…. first degree fam member should be tested too
Tx:
- copper chelating agents:
1. Trientine or D-penicillamine with B6
2. zinc supplements help to prevent uptake of dietary copper
3. liver transplant if unresp to therapy or liver failure
Kayser-Fleischer rings?
copper deposition in the cornea
–Wilson Dz
