failure to relax of LES, hypertonic at rest

no primary persistaltic waves in lower 2/3

• bird beak appearach
• no gas bubble in stomach
• dilated esophagus (megaesophagus)
• lengthenic of the esophagus

ulcerated, polypoid, infiltrative (+fungating)

infiltrative = linits plastica (=”leather bottle”, “scirrhous CA”) 📷

• inc. echogenicity (compare kidney)
• rounded borders (irregular margins)
• hepatomegaly (exceed upper liver pole)

→ may lead to fibrosis → cirrhosis

Chronic hepatopathy does not have a specific ultrasound aspect. In patients with chronic viral hepatitis B or C infection, hepatic steatosis is a frequent histological finding, occurring in more than 50% of cases.

The ultrasound findings in chronic hepatitis include:

1. Hepatomegaly (the lower border of the liver exceeds the upper pole of the kidney).
2. Steatosis (increased echogenicity of the liver compared to renal parenchyma).
3. Liver with rounded borders.
4. Increased diameter of the right lobe of the liver (normally less than 16 cm).

These findings suggest developing fibrosis and may indicate the possibility of malignant transformation, such as hepatocellular carcinoma.

hepatocellular carcinoma

HCC=early enhancement

cirrhotic nodule=enhanced together with liver parenchyma

normal blood clot doesnt have blood supply

HepC , Alcohol

• inc. ecogenicity (fat =hyperecho)
• portal veins not visible
• attenuation of US (due to fat)
• hepatomegaly
• homogenous echotexture,

• liver becomes more echogenic → no portal vein differentiation possible
• portal veins are usually differentiated due to their hyperechoic walls, → no differentiation possible

• heterogenous ecotexture (nodular micro/macro),
• +/- attenuation(due to fibrosis),
• no good deliniation of vessel (compression by the nodules),
• nodular contour/irregular margins,
• hepatomegaly or atrophy(when fibrotic tissue contracts)
• Portal HT (portal vein enlargement >12mm 📷, collaterals dilated)

portal HT / enlargement(>12mm)

• Inhomogeneous Echotexture: Normal liver has a fine, ordered appearance which is disturbed in cirrhosis, becoming irregular with mixed echogenic dots.
• Nodules: Presence of both micro-nodules (less than 3mm) and macronodules (greater than 3mm). The latter are regenerative nodules that are benign and have a well-defined appearance similar to the surrounding liver tissue.
• Surface and Architecture Changes: Irregular and nodular liver surface along with a loss of normal vascular structure within the liver.
• Liver Lobe Changes: Atrophy of the left and right lobes and hypertrophy of the caudate lobe are common in advanced cirrhosis.
• Portal Hypertension: Evidenced by an enlarged portal vein and reduced speed of blood flow within it.

• ascitis
• atrophy
• irregular, nodular, inhomogenous
• portal HT → HSM, porto-systemic shunts, ascitis

spleen, stomach (around cardia), abdominal esophagus

• reverberation (=air)

• encapsulated
• post-enhancement (liquid)
• irregular walls, but well deliniated

Doppler → incr. bloodflow in the periphery indicated inflammatory reaction

• oval
• regular walls/contour, well deliniated
• anechoic
• post. enhancement

• small (1-2cm)

→ hyperechoic

→ nodular

→ well deliniated

→ homogenous

→ no Doppler

→ typical enhancement with CM (see below)

• bigger

→ thrombotic areas

→ looks like a tumor

small, if it gets bigger destruction of capillarys, etc. looks like a tumor

metastasis! → complementary exam needed

rim enhance in portal/late phase (no washout → see video)

from periph → central region

regular periph. enhancement;

→ DD: metastasis

• nodular, well deliniated +margins
• black halo in periph
• Central: could be any color

• irregular peripheral enhancement
• irregular inner contour
• early washout

• large, heterogenous, poorly defined hyperechoic mass
• +- tumoral thrombosis

• vascular extend evaluation
• Uptake time (higher uptake + quicker washout in malignant lesion)
• extrahepatic diseases

Gadolinium

→ Hypersignal T1

→ Hyposignal T2

kidney → nephrotox

ARTERIAL PHASE

T1: compare to portal vein: cancer: early uptake; biliary metabolism: later uptake

early uptake → disproportial vascularization compared to portal vascularization

normal biliary metabolism take contrast up after 10-20min, malignancies → low bililary metabolism → very dark after 20min

40-60s

normal liver parenchyma → strong hypersignal

Metastasis, scar, cysts → black (hypovascular)

2-5min

gradually loses contrast

• Hemangioma → "wash in" begins here
• HCC → arterial early enhancement; inhomogeneous "wash out" hyposignal (in venous +late phase)→ evtl. with capsular hypersignal
• Cyst → no contrast uptake at all (compare to fluid in CSF)
• Adenoma → native T1: dark, Contrast → early uptake
• Focal nodular hyperplasia: Hyperintense in arterial phase with black scar tissue inside
• Metastasis: Hypersignal halo surrounding hyposignal lesion in arterial phase
• Abscess: Septa, fluid, necrotic tissue → no strong enhancement; compare also clinical picture

Fe (iron)

hyperintens on T2

dg of malignant metastasis → hypersignal on T2 [📷]

Primovist

hyperintense

differentiation HCC vs. Focal nodular hyperplasia vs adenoma

adenoma + HCC → hypointense in venous late phase(early washout)

FNH → hyperintense (dont wash out due to billiary metabolism)

HCC vs cirrhotic nodules → HCC early wash out, nodules no washout

Metastasis vs primary origin

📷:

• HCC
• FNH
• Adenoma

• multiple focal lesion
• incr. MDP uptake
• randomly asymmtric distributed, but around axial skeleton

hematogenous

• after breast + prostate cancer therpapy
• higher uptake in metastassis after chemo → good sign pentru ca osteoblastic response, bone healing

fracture → imagine fracture line → should be at the 2 sides of the fracture

• Hypertrophic Pulmonary Osteoarthropathy (HPOA) is characterized by the abnormal proliferation of the skin and the periosteal formation of new bone at the distal ends of long bones.
• Primary HPOA, 5% of cases ⇒ genetically inherited
• secondary HPOA, 95% ⇒ paraneoplastic syndrome. It is most commonly associated with advanced stages (III or IV) of adenocarcinoma lung cancer.
‣

💬

Secondary HPOA can also be linked to other conditions such as mesothelioma, renal cell carcinoma, gastrointestinal cancers, melanoma, thymic cancer, nasopharyngeal cancers, and Hodgkin lymphoma.

metastasis 📷

most probably due to fracture than metasis

osteolytic 📷

breast cc 📷

SPECT/CT

high uptAKE 📷 → further diagnostic needed: Three-Phase Bone scan

still high uptake of the sourroung → osteoblast try to heal

no good → better other techniques

osteoid osteoma: double density sign/headlight in fog 📷

no → i.v. bolus → start direct

• Te-99m DTPA - glomerular filtration
• Te-99 MAG3 - tubular secretion

you have to mark the ROIs (regions of interest)

x → time

y → measured radioactivity

Rise in the curve → progressive inflow of the tracer in the kidney = vascular phase

→ between min 2-5 → GF-phase (marked by the 2 yellow vertical lines)

⇒ then slow excretion phase

the 3 segments/phases (see one question above)

gap between the 2 lines is not important

45-55%

→ dosage card: 📷

• Obstruction severity
• surgical strategy
• efficiency of surgical treatment

true obstruction vs. "Lappen"-Obstruction ⇒ furosemid → incr. urinary pressure → in true obstruction is will still not flow like a river

basic renography + furosemid

→ wait 18min

⇒ rapid fall in curve → non obstructive

⇒ no/little fall → obstructive

Ectopic Kidney

horseshoe kidney

Vesicourethral reflux

multiple zones with no uptake in both kidney → smaller right kidney, with lesser uptake→ has probably suffered more (also 30%-70% split renal function)

Pancake kidney → no scarring in this case