18.9 Flashcards

1
Q

Describe the common gallbladder anomaly of phrygian cap

A

occurs due to the MC congenital anomaly of the GB due a folded fundus

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2
Q

besides the phyrgian cap anomaly, what other congenital anomalies are there

A
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3
Q

what is cholelithasis

A

>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.

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4
Q

what is the presentation of cholelithaisis

A

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)

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5
Q

what are complications of cholelithiasis

A

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

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6
Q

what population will you find pigmented stones

A

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

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7
Q

what are black pigmented stones and where do you find them

A

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

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8
Q

what are brown stones and where are they found

A

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

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9
Q

what are RF for pigmented stones

A

chronic hemolytic anemia

biliary infxn (C.sinensis, A.lumbricoides & E.coli),

GI d/o (CD, ileal resection, CF, etc)

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10
Q

what population present with cholesterol gallstones

A

more prevalent in the USA and W. Europ

75% prevalence rate in Native American populations (Pima, Hopi & Navajo)

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11
Q

what are cholesterol gallstones

A

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

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12
Q

what are RF for cholelithiasis

A

(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

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13
Q

what is the presentation of acute cholecystitis

A

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)

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14
Q

what is the range of severity of acute calculous cholecystitis

A

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

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15
Q

if there is a delay of treatment for acute cholecystitis what may occur

A

gangrene and perforation

Chance = acalculous > calculus

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16
Q

what population presents w/ acalculous cholecystitis

A

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

17
Q

how does chronic cholecystitis presetn

A

this will present w/ repeated episodes of acute cholecystitis (mild-severe)

but many times it develops in absence of antecedent attacks

18
Q

what complications may arise in either acute or chronic cholecystitis

A

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

19
Q

what’s the prevalence and characteristics of GB carcinoma

A

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

20
Q

what are the RF for GB carcinoma

A

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

21
Q

where do neoplasms of the GB spread to

why is there a poor prognosis

A

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