18.9 Flashcards
Describe the common gallbladder anomaly of phrygian cap
occurs due to the MC congenital anomaly of the GB due a folded fundus
besides the phyrgian cap anomaly, what other congenital anomalies are there
what is cholelithasis
>95% of biliary tract prob (10-20% adults)
GB affects 20 mill ppl in the US (700K get cholecystectomy)
There are two types: pigmented and cholesterol stones.
what is the presentation of cholelithaisis
Most remain asymptomatic, however convert to symptomatic at an avg rate of 4% per year
The risk of being symptomatic diminishes w/ times
The symptoms include pain after a fatty meal, esp in the RUQ and epigastric region, the pain may radiate to the R. shoulder
The pain may be due to inflammation from the stone (cholecystitis)
what are complications of cholelithiasis
Severe complications are empyema, perforations, fistula, cholangitis, obstructive cholestasis and pancreatitis
The smaller the stone, the more dangerous bc it can enter cystic duct or CBD and cause obstruction
Large stones can erode into adjacent small bowel loops and generate intestinal obstruction (gallstone ileus aka Bouveret syndrome)
increased risk of GB carcinoma if gallstones are present
what population will you find pigmented stones
non-western populations/Asian pts and rural populations
These are present in pts w/ bacterial/parasitic infxns of the biliary tree
or
pt w/ dz that lead to chronic RBC hemolysis
what are black pigmented stones and where do you find them
found in sterile GB bile
made of Ca2+ salts of unconjugated bilirubin, small amounts of Ca2+carbonate, Ca2+phos, mucin glycoprotein and some cholesterol
50-75% of the black stones are radiopaque due to the salts
what are brown stones and where are they found
infected large ducts
contain similar components as black stones but also some cholesterol and Ca2+ alkt of palmitate and stearate
radiolucent bc they contain Ca2+ soap
what are RF for pigmented stones
chronic hemolytic anemia
biliary infxn (C.sinensis, A.lumbricoides & E.coli),
GI d/o (CD, ileal resection, CF, etc)
what population present with cholesterol gallstones
more prevalent in the USA and W. Europ
75% prevalence rate in Native American populations (Pima, Hopi & Navajo)
what are cholesterol gallstones
100% cholesterol to 50% cholesterol
In the latter the rest is made up of Ca2+ carbonate, phosphates and bilirubin; these stones will look gray/white-black and may be laminated.
If all cholesterol = radiolucent (not seen on x-ray_
need some component of Ca2+carbonate helps to make stones radiopaque
what are RF for cholelithiasis
(6 Fs: F, 40, fair, fat, fertile and Fhx)
F, OC, estrogen exposure, pregnant,
obese/metabolic syndrome, fast wt loss,
GB stasis, inborn d/o if bile acid metabolism
HLD syndromes
what is the presentation of acute cholecystitis
90% are due to obstruction of the neck of the GB or the cystic duct
may have previous Hx of “attacks.”
progressive RUQ/epigastric pain (6 hrs) w/ fever, anorexia, tachycardia, sweating & N/V
labs = elevated WBC and mildly increased ALP. (no jaundice, but is hyperbilirubinemia then sign of obstruction of CBD)
what is the range of severity of acute calculous cholecystitis
mild symptoms that resolve on their own —– OR —– appear suddenly and need an acute emergency SRG (MC reason for emergency cholecystectomy)
It is imp to recognize this in severely ill pts bc of fatal outcome
if there is a delay of treatment for acute cholecystitis what may occur
gangrene and perforation
Chance = acalculous > calculus
what population presents w/ acalculous cholecystitis
systemic vasculitis
severe athersoclerotic ischemia in elderly
AIDS (related to cryptosporidium)
ascending biliary tree infxn
Rarely, there may be a primary bacterial infxn by S.typhi/staph
how does chronic cholecystitis presetn
this will present w/ repeated episodes of acute cholecystitis (mild-severe)
but many times it develops in absence of antecedent attacks
what complications may arise in either acute or chronic cholecystitis
bacterial superinfxn w/ cholangitis/sepsis
GB perforation and local abscess formation
GB rupture w/ diffuse peritonitis
biliary enteric (cholecystoenteric) fistula
aggravation of pre existing illnesses
what’s the prevalence and characteristics of GB carcinoma
MCC malignancy of the extrahepatic biliary tract
About 6K new cases every year in USA
women (2x)
Most = adenoCA and most often detected in the fundus
what are the RF for GB carcinoma
Most imp RF is gallstones (95% cases) BUT only 1-2% pts with gallstones will get CA
RF in Asia = chronic bacterial and parasitic infxns
where do neoplasms of the GB spread to
why is there a poor prognosis
usually invaded the liver and extended to the cystic duct and adjacent bile duct and portal hepatic LN by the time they are discovered, this is the reason for poor prognosis
The peritoneum, GI tract and lungs are common sites for spread
