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PoCUS > Liver & GB > Flashcards

Liver & GB Flashcards

1
Q

Cholecystitis

A
  • inflammation of the GB
  • multiple forms;

Acute cholecystitis
Acute acalculous cholecystitis
Chronic cholecystitis
Emphysematous cholecystitis
Gangrenous cholecystitis

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2
Q

Cholecystitis S&S

A
  • 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
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3
Q

Acute cholecystitis

A
  • 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

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4
Q

Acute cholecystitis US

A
  • 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
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5
Q

Acute acalculous cholecystitis (AAC)

A
  • 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

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6
Q

AAC US

A
  • GB wall >3mm
  • distended GB lumen > 4cm
  • positive Murphy’s sign
  • inc* colour Doppler flow in GB wall
  • pericholecystic fluid collection
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7
Q

Chronic cholecystitis

A
  • 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
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8
Q

Emphysematous cholecystitis

A
  • 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!!!
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9
Q

Emphysematous cholecystitis US

A
  • 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
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10
Q

Gangrenous cholecystitis

A
  • 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
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11
Q

Gangrenous cholecystitis US

A
  • 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
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12
Q

Cholestasis

A
  • 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

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13
Q

Cholestasis S&S

A
  • jaundice - skin & eyes
  • dark urine
  • light-coloured stools
  • generalised itching all over the skin

Cause dependant:
- abdominal pain
- loss of appetite
- vomiting
- fever

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14
Q

Cholestasis US

A
  • 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
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15
Q

Biliary sludge

A
  • 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
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16
Q

Cholelithiasis

A
  • 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)

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17
Q

Porcelain GB

A
  • 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

18
Q

GB adenocarcinoma

A
  • 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*
19
Q

Wall thickening

A
  • 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

20
Q

GB polyps

A

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

21
Q

Adenomyomatosis

A
  • 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*
22
Q

Scanning the GB

A

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

23
Q

Common bile duct US

A
  • 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)
24
Q

Fatty infiltration (Steatosis)

A
  • 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

25
Q

Non-alcoholic fatty liver Dx (NAFLD)

A
  • may or may not have assoc* inflamm*
  • non-alcoholic steatohepatitis (NASH)
  • assoc* w dyslipidaemia
  • can be reversed before NASH & scarring occurs
26
Q

Alcohol-related liver Dx (ALD)

A
  • preventable; can be reversed when stop drinking
  • ALS can lead to enlarged liver, alcoholic hepatitis, & alcoholic cirrhosis
27
Q

Diffuse Dx of Liver

A
  • 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

28
Q

Hepatitis

A
  • 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

29
Q

Hep A

A

Mode: faecal-oral
Class:
- picornaviridae
- linear
- SS-RNA
Incubation: 2-6 wks
Chronic Inf*: No
Clin outcomes of above: No

30
Q

Hep B

A

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

31
Q

Hep C

A

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

32
Q

Hep D

A

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

33
Q

Hep E

A

Mode: faecal-oral
Class:
- claviciviridae
- linear
- SS-RNA
Incubation: 21-42 days
Chronic Inf*: No
Clin outcomes of above: No

34
Q

Hepatitis S&S

A
  • fatigue
  • sudden nausea & vomiting
  • abdo pain/discomfort, esp RUQ
  • low-grade fever
  • dark urine
  • joint pain
35
Q

Hepatitis acute US

A
  • 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
36
Q

Hepatitis chronic

A
  • 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

37
Q

Hepatitis chronic US

A
  • 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

38
Q

Cirrhosis

A
  • 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

39
Q

Cirrhosis S&S

A
  • hepatomegaly
  • jaundice
  • ascites
  • nausea
  • anorexia
  • weight loss
  • dark urine
  • fatigue
  • varicosities
40
Q

Hepatic trauma

A
  • 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
41
Q

Glisson’s capsule

A
  • 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

PoCUS (14 decks)

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