Liver & GB Flashcards
Cholecystitis
- inflammation of the GB
- multiple forms;
Acute cholecystitis
Acute acalculous cholecystitis
Chronic cholecystitis
Emphysematous cholecystitis
Gangrenous cholecystitis
Cholecystitis S&S
- sharp/dull RUQ pain &/or epigastric area (Murphy’s sign)
- referred pain in/below R shoulder (diaphragm irritation)
- nausea & vomiting
- fever or chills
- chronic diarrhoea (non-acute Dx)
- jaundice
- unusual stools (clay-coloured) or urine
- above symptoms post fatty meal or at night
Acute cholecystitis
- usually caused by calculi blocking either the GB neck, cystic duct, or CBD.
- Can also be caused by other obstructions to the flow
Clin pres*:
- acute RUQ pain
- fever
- leukocytosis
- increased serum bilirubin & ALP levels
Acute cholecystitis US
- GB wall >3mm
- distended GB lumen > 4cm
- gallstones
- positive Murphy’s sign
- inc* colour Doppler flow in GB wall
- pericholecystic fluid collection
- impacted stone in GB neck, Hartman’s pouch or cystic duct
Acute acalculous cholecystitis (AAC)
- 10% of all acute cholecystitis cases
- main cause is GB dysfunction or stasis w stagnant bile
- more common in hosp* Pts (ICU)
- life-threatening cond* w a high risk of perforation & necrosis compared to cholecystitis invoking calculi
Clinical presentation
- same as acute cholecystitis but without elevated serum bilirubin & ALP levels
AAC US
- GB wall >3mm
- distended GB lumen > 4cm
- positive Murphy’s sign
- inc* colour Doppler flow in GB wall
- pericholecystic fluid collection
Chronic cholecystitis
- GB damaged by repeated attacks of acute inflamm*
- repeated attacks of acute cholecystitis & RUQ pain as calculi occlude the cystic duct/neck
- GB appearance may be thick-walled, scarred, & smaller in size
- note - lack of or minimal pericholecystic fluid
Emphysematous cholecystitis
- severe form of acute cholecystitis
- life- threatening anaerobic infection
- mortality rate: 15-20%
- assoc* w presence of gas-forming bacteria
- inc* risk of gangrene of GB wall & subsequent perforation
- surgical emergency!!!
Emphysematous cholecystitis US
- air in the wall/lumen of GB, in tissue adjacent to GB, or in biliary ducts
- if air is in GB it can appear like a WES sign
- it does ‘rise to the top’ so U can move the Pt on their side & check if gas has moved
- if air in intraluminal, bright ring down artifact
Gangrenous cholecystitis
- acute surgical emergency req* cholecystectomy
- serious complication of acute cholecystitis
- marked distribution of GB wall leads to increased tension
- inflamm* leads to progressive vascular insufficiency
- necrosis & perforation of the GB wall result
Gangrenous cholecystitis US
- thickened GB wall w de-lamination
- decreased blood flow in walls on colour Doppler
- gas within the GB
- may have an absence of calculi
- large pericholecystic collection
Cholestasis
- when bile flow ceases or reduced significantly
Can cause;
- acute hepatitis
- alcoholic liver Dx
- liver metastases
- cirrhosis due to viral Hep B or C
- blockage to bile duct (calculus, cholangiocarcinoma)
- primary biliary cholangitis
- pancreatic adenocarcinoma
- pancreatitis
- some drugs: amoxicillin/clavulanate, OCP
- cholestasis of pregnancy
Cholestasis S&S
- jaundice - skin & eyes
- dark urine
- light-coloured stools
- generalised itching all over the skin
Cause dependant:
- abdominal pain
- loss of appetite
- vomiting
- fever
Cholestasis US
- not visible on US per se
- can be attributed to causing: calculi formation, biliary sludge, & AAC
- must ask: how long have they had pain/presenting symptoms
- have they been eating normally up until now
Biliary sludge
- sludge, or thickened bile, freq* occurs from bile stasis
- may be seen in Pts w prolonged fasting, pregnancy, or obstruction of the GB
- can be seen as fluid line Or sludge ball that moves & has no vascularisation
Cholelithiasis
- most common Dx of GB
- single, large gallstone or multiple tiny stones
- Pts often fall under the 5 Fs: Fat, Female, Forty, Fertile & Fair
- other risk factors; pregnancy, diabetes, OCP use, cholesterol lowering meds, rapid weight loss, very low fat diets, over 60yrs, hypothyroidism & fam Hx
Whether they cause symptoms or not:
- largely depends on their size
- those that stay in the GB are relatively uncomplicated- May experience pain post w fatty meal as GB contracts if taking up big vol of space
- larger stones can get impacted in the GB neck if they happen to be there when the GB contracts - Mirizzi syndrome (pos* Murphy’s sign & severe RUQ pain)
- WES possible (Wall Echo Shadow sign)
Porcelain GB
- calcifications within the GB wall
- usually consists of diffuse intramural calcifications
- low assoc* w GB carcinoma (6%)
S&S:
- often non-specific symptoms
- abdo pain
- may have nausea & vomiting, jaundice, &/or fever
GB adenocarcinoma
- about 85% of all GB CAs
- develop within the mucus memb* in GB
- uncommon overall but needs to be considered for DDx
- Pts w Hx of gallstone & GB inflamm* are more likely to develop these
- FHx GB CA increases risk 5-fold
- S&S - same as other GB path*
Wall thickening
- may be acute & inflammatory, or chronic w minimal inflammation
- seen in a lot of the GB conds
Maybe assoc*:
- ascites
- GB wall abscess
- hepatitis or cirrhosis
- RHF
- multiple myeloma
- portal node lymphatic obstruction
- hypoalbuminaemia
GB polyps
3 types:
Pseudopolyps/cholesterol polyps: 60-90% of all GB polyps, cholesterol
-filled growths, often accompanying other GB (benign)
Inflamm* polyps; 5-10% of GB polyps, extensions of inflamed GB wall, usually found in ppl w have Hx cholecystitis >1 x or have acute biliary colic (benign)
True GB polyps: rare, may become malignant, usually measure 5-20mm, cholecystectomy recomm* when lge polyps present
Adenomyomatosis
- most Pts >40yo
- 3:1 - female: male
- hyperplasia of GB wall
- formation of Rokitansky-Aschoff sinuses (intramural diverticula lined by mucosal epithelial cells
- crystals from the RA sinuses (comet-tail artifact)
- unknown cause
- incidental finding & No Rx req*
Scanning the GB
Low freq* probe
- 1-6 MHz sector or curved array
Basic parameters adj* while scanning
- depth
- gain
- focus (if equip* allows)
Pt must be fasted to visualise a distended GB (min 6 hrs)
GB must be scanned in variable positions
US:
- wall thickness <3 mm
- lumen - anechoic
- shape - pear
- size - variable w fasting period
- fasting GB length approx 10cm
- often easier to see when Ot rolled 30-45 degrees to L
Common bile duct US
- echogenic GB & duct walls
- IVC & portal vein behind GB
- +/- Doppler confirms portal vein flow
- GB under visceral surface of the liver, in front of the duct
- be careful not to confuse hepatic artery & the CBD (closely positioned & similr size) Apply colour Doppler to differentiate
- normal size up to 6mm (can be 1mm larger every decade past 60yo)
Fatty infiltration (Steatosis)
- build up of fat in >5% of liver cells
- non-alcoholic & alcoholic
Mild: minimal diffuse increase in hepatic echogenicity
Mod: increased echogenicity w slightly impaired visualisation
Severe: sig* increase in echogenicity of liver parenchyma & decreased penetration
Visualisation:
- diffuse/focal
- fatty sparing
Non-alcoholic fatty liver Dx (NAFLD)
- may or may not have assoc* inflamm*
- non-alcoholic steatohepatitis (NASH)
- assoc* w dyslipidaemia
- can be reversed before NASH & scarring occurs
Alcohol-related liver Dx (ALD)
- preventable; can be reversed when stop drinking
- ALS can lead to enlarged liver, alcoholic hepatitis, & alcoholic cirrhosis
Diffuse Dx of Liver
- diffuse hepatocellular Dx affects the hepatocytes & interfered w liver function
- hepatocyte is a parenchymal liver cell that performs all the functions of the Liver
- diffuse Dx is measured via liver function tests
- hepatic enzyme levels are elevated w cell necrosis (tissue death)
Chronic hepatitis => cirrhosis => hepatocellular carcinoma w cirrhosis
Hepatitis
- inflamm* of liver
- acute or chronic
- most commonly caused by viral infection
- other causes; autoimmune hepatitis, hepatitis secondary to meds, drugs, toxins & alcohol
Types:
Hep A - found in faeces of infected Pts
Hep B - spread thru infected body fluids
Hep C - most serious type & spreads thru blood
Hep D - can only be contracted if U have HBV
Hep E - transmitted via food & water
Hep A
Mode: faecal-oral
Class:
- picornaviridae
- linear
- SS-RNA
Incubation: 2-6 wks
Chronic Inf*: No
Clin outcomes of above: No
Hep B
Mode: blood borne, sexual, vertical
Class:
- hepadnaviriae
- circular
- DS-DNA
- R.T enzyme
Incubation: 2-6 months
Chronic Inf*: Yes 10%
Clin outcomes of above:
- cirrhosis or hepatocellular carcinoma
Hep C
Mode: blood borne
Class:
- flaviviridae
- linear
- SS-RNA
Incubation: 2 wks - 6 months
Chronic Inf*: Yes 60-80%
Clin outcomes of above:
- cirrhosis or hepatocellular carcinoma
Hep D
Mode: blood borne (depend on HBV), super or co infection
Class:
- deltaviridae
- circular
- SS-RNA
Incubation: 60 - 180 days
Chronic Inf*: Yes
Clin outcomes of above:
- co-infection
Hep E
Mode: faecal-oral
Class:
- claviciviridae
- linear
- SS-RNA
Incubation: 21-42 days
Chronic Inf*: No
Clin outcomes of above: No
Hepatitis S&S
- fatigue
- sudden nausea & vomiting
- abdo pain/discomfort, esp RUQ
- low-grade fever
- dark urine
- joint pain
Hepatitis acute US
- liver texture may appear normal, or portal vein may appear more prominent than usual
- liver parenchyma is slightly more hypoechoic due to swelling of liver cells via inflamm*
- inc* ‘brightness/prominence’ of the portal veins (star effect)
- attenuation may be present
- hepatosplenomegaly is present
- GB wall thickened
Hepatitis chronic
- may be asymptomatic
- can progress to fibrosis & cirrhosis (scarring) & liver failure
2 types:
- chronic persistent Hep; benign self-limiting process
- chronic acute Hep; usually progresses to cirrhosis & liver failure
Hepatitis chronic US
- liver parenchyma is coarse & more echogenic/hyperechoic due to fibrosis
- portal vein walls are less discrete compared to the more reflective parenchyma
- liver does not inc* in size w chronic Hep
- fibrosis may be evident; may produce ‘soft shadowing’ posteriorly
- changes to liver contour
HCV infection => chronic Hep => 20-25yrs cirrhosis => 25-30yrs HCC, ESLD, death
Cirrhosis
- permanent scarring of liver where normal liver tissue is replaced by scar tissue
4 types;
- alcoholic (Laennec’s)
- post-necrotic
- biliary
- cardiac
3 nodule types;
- micronodular cirrhosis
- macronodular cirrhosis
- mixed cirrhosis
Cirrhosis S&S
- hepatomegaly
- jaundice
- ascites
- nausea
- anorexia
- weight loss
- dark urine
- fatigue
- varicosities
Hepatic trauma
- laceration can occur from blunt or penetrating trauma
- haematoma can occur around &/or within liver following trauma (esp after Lac)
- R love affected more then L
Glisson’s capsule
- inner layer of connective tissue layer over liver & surrounding the portal triad within the liver
- outer layer of liver capsule is the peritoneum
- can be cause if RUQ pain w an enlarged liver
