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acute cholecystitis
stone (95% of the time) is in the cystic duct, leading to biliary colic - when it’s without stones, the condition is called acalculous cholecystitis
hepatolithiasis
stone in intrahepatic and extrahepatic bile ducts, causes cholangitis, which is bacterial infection of biliary tree
chronic cholecystitis
long-standing gallbladder inflammation, usually the result of gallstones and prior acute cholecystitis attacks - marked by repeated attacks of pain (biliary colic) that occur when gallstones periodically block the cystic duct
what can happen with repeated attacks of acute inflammation of the gallbladder
gallbladder may become smaller and its walls may become thick and scarred, gallstones may block the opening of the gallbladder into the cystic duct or block the cystic duct itself, gallbladder usually contains sludge, porcelain gallbladder may occur
what is it called when gallbladder scarring becomes so extensive calcium is deposited in the walls of the gallbladder?
porcelain gallbladder
cholesterol gallstones
make up more than 80% of gallstones in the US - due to amount of cholesterol secreted by the liver cells, relative to lecithin and bile salts and the degree of concentration and extent of bile stasis
calcium, bilirubin, and pigment gallstones
bilirubin is the yellow pigment from the breakdown of heme and unconjugated bilirubin may be higher than normal (creates crystals)
mixed gallstones
cholesterol gallstones colonized with bacteria, causing mucosal inflammation and stones accumulate calcium bilirubinate and other salts
cholesterol as a risk factor for fallstones
more common in females, European or Native American ancestry, and with increasing age - obesity (from metabolic syndrome) - pregnancy (multiple, high-testosterone levels reduce gallbladder contractility, leading to prolonged retention) - gallbladder stasis (high spinal cord injuries, prolonged fasting with parenteral nutrition, rapid weight loss from gastric bypass) - heredity - medications (estrogen-based contraceptives, prostate cancer treatment, some hypolipidemic drugs and somatostatins)
black pigment stones
due to high heme turnover - about 10-20% of gallstones in the US
brown pigment stones
intraductal stasis and chronic colonization of bile with bacteria - in the US it’s most common with postsurgical strictures or choledochal cysts - in East Asia ot’s most common with infestation of biliary flukes
cholelithiasis on imaging
appears round or oval, smooth or faceted, radiodense shadow sin the RUQ in the frontal view and anterior to the spine in the lateral view - best identified by ultrasound - oral cholecystography involves use of oral contrast agent to opacify gallbladder (not commonly used)
are plain x-rays good for viewing gallstones?
no, only 10-15% contain enough calcium to be visible on plain films
cholelithiasis
stones are often asymptomatic (only 10% develop symptoms within first 5 years of finding stones) - attacks of pain often follow ingestion of fatty meals, and may occur at night, consist of steady pain in RUQ that increases rapidly and lasts from 30 minutes to several hours, pain in the back between shoulder blades, and pain in right subscapular region - there is concern for duct obstruction and infection - intervention includes laparscopic surgery and lithotripsy
causes of hepatomegaly
cirrhosis, carcinoma, congestive heart failure, infection (viral hepatitis), immune (primary biliary sclerosis), infiltrate (NAFLD - nonalcoholic fatty liver disease now called metabolic dysfunction associated steatotic liver disease)
hepatomegaly
for the adult liver, the midclavicular line averages 19012.5 cm in craniocaudal length - average transverse diameter is 20-23 cm at the level of the upper pole of the right kidney - look for extension of the right lobe inferior to the lower pole of the right kidney and rounding of the hepatic inferior border
when is a liver considered enlarged
when a liver is longer than 15.5-16 cm in the midclavicular line
reidel lobe
a normal variant of the liver with a large right hepatic lobe - liver extends past the inferior lobe of the right kidney but nothing is displaced
possible reasons for splenomegaly
infectious disease, anemias, tumors, portal hypertension, and sickle cell disease - splenomegaly can displace the left kidney
nephrolithiasis
concretion calcification in the luminal portion of the urinary tract, secondary to urinary stasis or lack of volume (prevalence about 10%) - 90% of these are visible on radiographs and sometimes they have a ‘staghorn’ appearance - low back pain, flank pain (ureteric colic) due to urinary obstruction - associated with increased uptake of calcium, calcium oxalate, uric acid or salt in our diet or with an inadequate intake of fluids
what’s the best imaging for looking at kidney stones?
CT - ultrasound is likely the first form of imaging but CT and intravenous pyelogram would be confirmatory tests
what other small calcification within the pelvic basin could you confuse for a renal calculus?
phleboliths - usually form below the femoral heads and the ureters connect to the bladder about them
staghorn stone
fills both the renal pelvis and calyces
diet risks for nephrolithiasis
tea, high protein, rhubarb, chocolate, peanuts, and spinach (high in oxalates)
kidney stones less than what measurement are usually passed without surgical intervention?
5 mm
simple renal cyst type I
thin walled, no septae calcifications, or enhancement - no risk of malignancy - no treatment
simple renal cyst type II
few hair-line septae, fine calcifications, may be high-attenuation cysts <3 cm - minimal risk of malignancy - no treatment
minimally complex renal cyst type II F
multiple hair-line septae, minimal smooth thickening of wall or septa, may have thick calcifications but no enhancement, cysts >3 cm - 3-10% chance of malignancy - surveillance
complex renal cyst type III
thicker or more irregular walls with measurable enhancement - 50% risk of malignancy - surgical excision is treatment
clearly malignant renal cyst type IV
class III+ enhancing soft-tissue components - 75-90% malignancy risk - surgical excision is treatment
bladder calculi
formed from urinary stasis, usually due to obstruction or inability to empty the bladder - more than 80% occur in elderly males - associated with carcinoma (squamous cell carcinoma) - usually oval radiodense shadows in the bladder, but often not fully opaque (may result in lamination) - related to infection secondary to irritation of the bladder wall - most common type of stone is made of uric acid (but don’t think about gout)
chronic bladder infections
can lead to stones AND may be secondary tp irritation of the bladder wall by the stone
squamous cell carcinoma of the bladder
RARE - associated with bladder stones, recurrent UTI, bladder outlet obstruction, long-term indwelling catheters
factors that promote uric acid stone formations
persistently low urinary pH, dehydration leading to low urinary output, and high uric acid production
uterine fibroma
seen in 40% of women over 35 years - intramural, subserosal, or submucosal locations - plain films may demonstrate ‘popcorn’ or ‘cauliflower’ calcification - most fibroids are asymptomatic and of little concern - problems arise with bleeding, mass effect on viscera, infertility, and malignant degeneration (3%)
aortic and iliac anatomy
abdominal aorta has 3 separate tissue layers (intima, media, adventitia) - the diameter of the (normal) aorta decreases from its thoracic portion to its abdominal and infrarenal portions - most AAAs begin caudal to the renal arteries and cephalic to the iliac arteries - normal aorta is lass than 3 cm on a lateral radiograph
dilation
refers to the act of becoming wider, larger, or more open - physiologic
dilatation
refers to the action of being dilated beyond normal dimensions - pathologic
what are the different shapes an AAA can have?
fusiform (oval), saccular (bubble hanging off artery), spectrum (like a sickle cell)
what shape of an AAA is more likely to burst?
saccular
the healthy aorta dimater is influenced by
age, sex, height, and body habitus
aneurysms
focal dilation in n artery, with at least a 50% increase over the vessel’s normal diameter
AAA prevalence
most common arterial aneurysms - usually occur in those over 50 years (prevalence increases as age increases) and more common in men - higher prevalence in western countries than Asian countries, higher in Australia than US and Europe - SMOKERS, hypertension, hyperlipidemia, hereditary, atherosclerotic occlusive disease
AAA concerns
silent until expansion impacts distal and adjacent structures (intrinsic and/or extrinsic compression) if diagnosed early, treatment of risk factors and contributing illnesses can be addressed - if ruptured, has a mortality rate of 59-90% outside of a hospital setting - emergency operative mortality rates are 40%, elective surgical repair rates are much lower (5-5.9 cm size)
AAA signs and symptoms
vague, but persistent and deep back pain abdominal pain (possible extension to the flanks and groin) - pulsatile umbilical pain (maybe only with palpation)
ruptured AAA signs and symptoms
abdominal pain, back pain (could mimic renal calculi), groin, buttock, leg, and scrotal pain, tachycardia, dizziness with standing, syncope, sweaty/clammy skin, nausea, vomiting, periumbilical ecchymosis (cullen sign), flank ecchymosis (grey turner sign)
abnormal abdominal aorta measurements
diameter larger than 3.5-4 cm or if there are any focal contour changes (saccular) - the larger the vessel, the more likely it is to rupture
AAA surveillance - imaging
radiography depends on presence of calcification, but calcification is only seen in 50-85% of cases - ultrasonography is nearly 100% accurate (and preferable) - CT demonstrates excellent detail and is used for surgical mapping - arteriography (angiography/contrast study)
AAA surgical repair
won’t usually happen if not <5.5 cm, but maybe less for women, if symptomatic, if rate of growth expands by more then 0.5 cm in 6 months, if the AAA form is saccular, if there is a family history of AAA - done with stenting
intraluminal gas pattern
normal and expected in stomach and bowel, abnormal is gallbladder portal vein, and urinary bladder - recognition of displacement of normal bowel gas distribution due to pathology like ascites or masses
extraluminal gas pattern
always abnormal - most commonly found within the peritoneal cavity (air in urinary bladder is often due to infection)
intramural gas pattern
seen in walls of abdominal cavity - always abdominal
abscess gas pattern
always abnormal
intraluminal bowel obstruction causes
small bowel obstruction is most common - paralytic ileus or adynamic ileus - large bowel could be sigmoid or cecal volvulus, colitis, or gastric outlet obstruction - gallstone ileus with the biliary tree - ischemic bowel
examples of extraluminal bowel gas
perforation (intra or extra peritoneal) - pneumatosis coli, ischemic bowel, and gas-forming infections can cause intramural gas
small bowel obstruction
radiographic findings MAY be apparent 6-12 hours BEFORE the clinical symptoms - abdominal pain, vomiting, distention, dilated loops of small bowel, air-fluid levels, small bubbles trapped between bowel loops (string of pearls), fluid-filled loops = gasless abdomen but that’s less common
normal diameter for small intestine
less than 30mm/3cm for proximal (jejunum) and less than 25mm/2.5cm for distal ileum
abnormal air-fluid levels for small intestine
more than 25mm/2.5cm in length (span) and if they are at different positions in the same loop (creating step-ladder appearance)
mechanical small bowel obstruction
most common cause of all intestinal obstructions (about 80% are small bowel) - due to post-surgical adhesions in western countries, incarcerated hernias (so include inguinal regions on abdominal and LP x-rays), gallstone ileus, foreign bodies, intussusception, intraluminal masses, malignancy
paralytic ileus/adynamic ileus
stasis of the bowel contents WITHOUT mechanical obstruction - causes can be postoperative, drugs, metabolic states, intra-abdominal inflammation
abnormal gas pattern findings for small bowel obstruction
central location, stacked coins appearance due to valvulae conniventes extending from wall to wall - accumulations suggest obstruction from adhesions secondary to intra-abdominal surgery, hernias, tumors, and Crohn’s disease
abnormal gas patterns for large bowel obstruction
normally air in the rectum an sigmoid colon, so peripheral location - haustral markings don’t extend from wall to wall
abnormal gas pattern for the stomach
enlargement OR displacement of the usually small amount of gas in the fundus (medial, lateral, and upward)
3 6 9 diameter rule
small bowel should be <3 cm, large bowel should be <6 cm, appendix should be <6 cm, cecum should be <9 cm