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472 Cards in this Set
- Front
- Back
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What is the Vas Deferens?
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The communicationbetween the epididymisand the ejaculatory ducts. The vas or ductus deferenstravel through the inguinalcanal, cross superiorly tobladder, travel mediallyand inferiorly to unite withthe seminal vesicles toform the ejaculatory duct.
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What are the seminal vesicles? Where do they lie in the pelvis?
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The seminal vesicles lie posterior to the urinarybladder, superior to theprostate. the Vas Deferens & Seminal Vesicles form theejaculatory duct, traversingthe prostate to enter theurethra at theverumontanum Contribute 60% of the volume of semen.
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What do the seminal vesicles secrete?
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Seminal vesicle secretes fluid that contains ATP, prostaglandins, clotting factors, proteins, etc. which contributes to the volume of the semen.
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What is the prostate gland?
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Small, round, muscularorgan • Diameter~4cm• Surrounds the prostatic urethra • Produces a weak acidicsecretion accountingfor 20-30% of thesemen volume.
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What are the zones of the prostate?
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Peripheral, central, transition, periurethral glandular area, and anterior fibromuscular area.
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What is the peripheral zone?
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The largest prostate zone, accounting for 70% of the glandular tissue. Occupies the posterior, lateral, and apical regions. This is the most common site of prostate cancer. A SURGICAL CAPSULE separates it from the transition and central zones.
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What is the Central Zone?
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The Central zone accounts for 25% of the glandulartissue and sits superior (by thebase), posterior &lateral. Wedged in the midlinebetween theperipheral & transitionzones VD and SV enter here. This area is relatively resistant todisease processes**
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Which zones make up the inner gland?
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The transition zone, fibromuscular stroma, periurethral glands, and the capsule.
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What is the transition Zone?
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Contains 5% of the glandular tissue, and completely surrounds the urethra. The verumonatnum is the inferior border. This is where BPH orriginates**
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What is the fibromuscular stroma?
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Not glandular tissue and therefore little pathology occurs here.
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What are the periurethral glands?
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Embedded in the smooth muscle of the proximal urethra.
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What is the capsule of the inner gland of the prostate?
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Formed by periprostatic soft tissue (muscle and connective tissue).
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What is TRUS used for in females?
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TRUS - trans rectal ultrasound
In females it is used to assess for cancers, or other rectal pathology (similar to males but for males it also assesses for prostate cancer). |
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What does the prostate look like using TRUS?
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The prostate will appear ovoid in shape in both longand trans • Homogeneous • Peripheralzoneusedasstandard forechogenicity - considered isoechoic.
PERIURETHRALAREA:– HYPOechoic Anterior FibromuscularStroma = HYPERechoic Surgical capsule maybedifficult to identify;becomes more evidentwith BPH -> ‘CorporaAmylacea’ |
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What is the approximate normal size of the prostate?
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4 (trans) x 3 (AP) x 3 (long) x 0.523 cc
In younger patients their prostate should be less than 20, in older patients more than 40 grams would be considered enlarged. |
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What is corporea amylacea?
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Proteinaceous material indigenous to the prostate, a precursor of calculi formation. It will appear hyper echoic on ultrasound, with an eiffel tower appearance along the prostatic urethra.
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Explain the vascularity of the prostate gland.
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Supplied by the prostaticovesical artery (branch of IIA). It is important to see blood flow within the prostate gland. However, it is not helpful for diagnosis (increases with neoplasias, and inflammation).
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How will the prostate look on TA ultrasound?
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IT will demonstrate the gross anatomy only, with no parenchymal detail. The seminal vesicles will look like a bow tie.
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What are most prostatic cysts caused by?
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Parenchymal degeneration in hyperplastic nodules OR a retention cyst.
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What are the 6 categories of prostatic cysts?
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– Parenchymal cysts
– Isolated medial cysts(Utricle & mullerian) – Ejaculatory duct cysts – Abscesses – Cystic tumors – Parasitic |
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What is a mullerian duct cyst?
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Midline, lateral and large cyst with no spermatozoa or other associations.
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What are prostatic utricle cysts?
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Midline, small cysts associated with unilateral renal agenesis, hypospadias, and cryptorchidism.
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What are ejaculatory duct cysts?
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Small, along the ejaculatory duct, fusiform, contain spermatozoa and can cause perineal pain.
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What is a seminal vesicle cyst?
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Large, solitary cyst, a wolffian duct anomaly associated with ipsilateral renal/testis agenesis, ADPKD.
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What is Benign Prostatic Hypertrophy?
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Glandular hyperplasia of >40 grams. There is a spontaneous occurrence in men over 50 years old. The hyperplasia occurs in the transition zone, causing encroachment of the urethra.
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What are the clinical presentations of BPH?
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Urinary frequency, nocturia, dribbling (difficulty starting and stopping flow), and slightly elevated PSA.
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What the the sonographic features of BPH?
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Enlarged gland (>40 grams), hypoechoic enlarged inner gland, heterogenous appearance, possible calcifications, and nodules and/or cysts in the transitional zone.
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What are the possible complications of BPH?
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- Hydronephrosis
- stones - thick bladder wall - bladder diverticula - trabeculated bladder |
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How do you treat BPH?
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- Blood pressure drugs
- testosterone-inhibiting drugs and herbs - TURP - transurethral retrograde prostatectomy |
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What is an indication that a patient has undergone a TURP procedure?
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Collapsing of the gland in on itself.
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What is prostatitis?
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Refers to a chronic pain syndrome (inflammation and infection).
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What are the 4 categories of prostatitis?
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(1) Acute bacterial
(2) Chronic bacterial (3) Chronic prostatitis/chronic pelvic pain syndrome (inflammatory and noninflammatory cases) (4) Asymptomatic inflammatory |
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What is acute/chronic bacterial prostatitis? Treatment?
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Uncommon, bacterial infection of the prostate by E.coli most commonly. This can be treated with antibiotics?
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What is chronic prostatitis/chronic pelvic pain syndrome?
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Most common form of prostatitis and the most difficult to understand and treat. Inflammatory is type A where there are WBCs in the secretions, and the nine-inflammatory is type B (prostatodynia) - unknown etiology.
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What are the clinical presentations of prostatitis?
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- Pain ** (in the lower back, perineum, and rectum)
- Fever - Painful urination - Mucousy discharge (containing WBCs) - Hematospermia (in the chronic form) |
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What are the sonographic features of acute prostatitis?
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- Hypoechoic gland
- Geographic hypo echoic areas - Increase in gland size - increase in vascularity |
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When might abscess occur with prostatitis? SF?
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Most commonly it will happen in acute prostatitis, or diabetic patients.
SF: anechoic mass with or without internal echoes. |
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What are the sonographic features of chronic prostatitis?
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- Focal masses of variable echogenicity
- Ejaculatory duct calcifications - Capsular thickening or irregularity - Periurethral gland irregularity - Distended seminal vesicles |
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What is a differential diagnosis for prostatitis?
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Prostate Cancer
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Why is prostate cancer considered so dangerous?
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The most commonly diagnosed cancer in men, and highest cause of death in men >75 years old.
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What is the most common form of prostate cancer?
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Adenocarcinoma
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What is the aetiology of prostate cancer?
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Exact etiology is unknown but it is hormone related (testosterone)
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How commonly does prostate cancer develop in each of the prostatic zones?
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70% occur in the peripheral zone
20% occur in the transitional zone 10% occur in the central zone |
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When does screening for prostate cancer begin?
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Starts at 50 years of age, and includes digital rectal exam and a PSA.
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What is the main purpose of TRUS for the diagnosis of prostate cancer?
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It is not for diagnosis, it is not sensitive enough to be used alone for detection and diagnosis, it is used to guide biopsies and/or therapies.
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What is PSA?
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Prostatic-specific enzyme, which is an enzyme normally excreted by the epithelial cells of the prostate ducts, some of which leaks into the blood and can be measured.
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What is the function of PSA?
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To help liquify the ejaculate
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What are normal serum levels of PSA?
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<4 ng/mL
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How is the PSA level different in cancer patients?
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Cancer typically is associated with 10x the normal PSA levels; however, 10-20% of men with prostate cancer have normal serum levels of <4ng/mL
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In what conditions (other than prostate cancer) may PSA levels rise?
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BPH, inflammation, DRE, biopsy, cystoscopy
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What are the clinical presentations of prostate cancer?
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- Asymptomatic
- Men > 50 - Abnormal PSA (>10) - Palpable mass on digital rectal exam - may have urinary or reproductive symptoms (hematospermia, low amounts of ejaculate) - Pain (related to bony metastases) |
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What are the SF of prostate cancer?
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- Focal Small Nodule: hypoechoic*, or isoechoic (in transitional zone); look for asymmetry or capsular bulging
- Focal Large Nodule: Hyperechoic (uncommon) - Diffuse: difficult to detect - if peripheral zone related it will be hypo to the inner zone, and the entire gland is replaced it will be hypo to normal. If the entire gland is replaced and there is hyperplasia then it will be inhomogeneous. |
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How do you treat prostate cancer?
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Depending on age: watchful waiting (if in an older man), radical prostatectomy, or radiation therapy (external beam or brachytherapy).
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Explain the location and the make-up of the thyroid gland.
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Located in the lower neck anterior to the trachea, and the esophagus. The two lobes are connected by an isthmus, there may also be an additional pyramidal lobe (seen commonly in young children).
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What are the lobes of the thyroid?
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2 lateral lobes, a connecting isthmus, and a pyramidal lobe (seen in young children).
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What are the muscles that surround the thyroid gland?
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Surrounded by muscle anteriorly by the sternocleidomastoid, omohyoid, sternohyoid, and sternothyroid.
Surrounded posteriorly by the anterior scalene, and the longus colli (runs parallel along the spine from C1 to T3). |
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What is the major NVB?
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Consists of carotid sheath and its contents: CCA, IJV, and the vagus nerve.
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What is the minor NVB?
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Consists of inferior thyroid artery, and the recurrent laryngeal nerve.
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How do muscle bundle appear sonographically?
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The Thyroid Gland Normal muscle bundles are HYPOechoic with hyperechoic bands of fibroadipose striations
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How will the trachea appear on a sonogram?
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Cresent shaped hyaline cartilage, anterior to the spine, and monographically the echogenicity is similar to bone.
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How will the esophagus appear in a sonogram?
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Collapsible muscular tube, posterior to trachea, and anterior to spine. It is located left of the midline.
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What is the normal size, shape, echogenicity, and contour of the thyroid sonographically?
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Size: lateral lobe - 4-6cm in length, 3-6 cm in width, 1.4-1.8 cm AP. The Isthmus - 4-6 mm AP
Shape: ovoid Echogenicity: very homogenous, med-high echogenicity Contour: smooth (capsulated) |
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When will the size of the thyroid increase?
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It will increase in size symmetrically in youth, females (hormonal), and we-nourished individuals.
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What arteries supply the thyroid?
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It is very vascular and is supplied by the ITA, and the SPA.
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What are the vessel sizes in the thyroid?
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Arteries: 1-2mm
Veins: up to 8mm |
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What is the lymphatic drainage of the thyroid like?
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Drainage is to the deep nodes: jugular and mediastinal.
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What are some congenital anomalies of the thyroid?
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- Agenesis (lobar or whole gland)
- Hypoplasia (decrease in gland size) - Ectopia |
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What makes up 70% of congenital anomalies of the thyroid gland?
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Thyroglossal duct remnants or cysts.
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Explain what a thyroglossal duct remnant is.
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The thyroid gland begins as a diverticulum of the pharynx that descends to its normal location. The thyroglossal duct is the temporary communication between this diverticulum and the tongue.
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What is a thyroglossal duct cysts?
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a remnant of the duct that did not remain temporary.
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Sonographically what do thyroglossal duct remnants/cysts look like?
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Located midline (anywhere between the base of the tongue and the thyroid isthmus) and may be anechoic or have some internal echoes (if infected). The cyst will be medial to the strap muscles.
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How will a thyroglossal duct cyst present clinically?
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If symptomatic, it will present in the paediatric stage. Clinical presentation may include: palpable mass, visible mass, dysphagia, and pain.
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What are brachial cleft cysts?
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A branchial cleft cyst is a congenital epithelial cyst that arises on the lateral part of the neck due to failure of obliteration of the second branchial cleft (or failure of fusion of the second and third branchial arches) in embryonic development.
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What is the clinical presentation of brachial cleft cysts?
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Palpable lateral neck mass, tender if infected.
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What is the treatment of a brachial cleft cyst?
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Antibiotics or surgery
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What do brachial cleft cysts look like sonographically?
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simple cyst - pseudo solid with some internal debris (infection) and posterior enhancement.
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What is a cystic hygroma?
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A congenital modification in the cervical lymphatic system causing thin walled cystic masses in the neck.
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What percentage of cystic hygromas are associated with congenital abnormalities?
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60%
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What is the most common location for a cystic hygroma?
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occipital region
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Explain the parathyroid glands?
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Posterior to the thyroid, usually in 2 pairs - superior and inferior. They may be intra or extra thyroid capsule and the inferior ones tend to be ectopic.
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What is the common size of a parathyroid gland?
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5 (L) x 3 (W) x 1 (AP) mm
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What do parathyroid glands look like sonographically?
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homogenous
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Why does renal failure affect most of the body's systems?
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Due to its important role in:
- Maintaining fluid balance - Regulating the electro-chemical composition of body fluids - Regulating acid-base balance - Controlling blood pressure |
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What are the categories of renal failure?
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Acute, Chronic and Acute on Chronic
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What does renal failure result in?
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Azotemia (medical condition characterized by abnormally high levels of nitrogen containing compounds in the blood largely related to problems with filtering in the kidneys).
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What happens to a patient who is suspected of acute renal failure (why are they suspected)?
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If someone's creatinine levels are suddenly increased they will be sent for an ultrasound for screening. A renal biopsy will need to be performed if parenchymal destruction is seen to determine actual cause.
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What are 3 possibilities for increased creatinine levels?
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- Mechanical obstruction of flow out of the kidneys
- Renal parenchymal destruction - Decreased blood flow to the kidneys |
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Explain the prerenal causes of acute renal failure. What are 3 causes?
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M/C form of acute renal failure characterized by a marked decrease in renal blood flow.
Causes: - Hemorrhage - Heart failure - Anaphylaxis or sepsis |
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Is a prerenal cause of acute renal failure reversible?
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Yes if the cause of decreased blood flow can be identified and corrected early.
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What are the postrenal causes of acute renal failure?
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Results from obstruction (in ureter, bladder, or urethra) of urine outflow from the kidneys. Necessary to treat the cause before permanent kidney damage occurs.
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Is a postrenal cause of acute renal failure reversible?
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Yes! It is necessary to treat the cause before permanent kidney damage occurs.
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What are the intrinsic or internal causes of acute renal failure?
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Results from conditions that cause damage to structures within the kidney - medical renal disease.
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What are examples of medical renal disease?
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- Acute Tubular necrosis
- Acute cortical necrosis - Glomerulonephritis - Acute interstitial nephritis - Diabetes Mellitus |
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What is acute tubular necrosis? What are the causes?
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Destruction of the tubular epithelial cells due to toxic or ischemic insults:
- Hypotension - Overwhelming sepsis - Trauma - Dehydration - Drugs |
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What is the most common cause of acute reversible renal failure?
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Acute Tubular Necrosis
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What are the clinical presentations of acute tubular necrosis?
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- Non-concentrated urine
- Sharp decrease in urine output - Very sick patients |
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What are the sonographic features of ATN?
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Depends on the cause:
- Ischemic (hypotensive) - normal - Toxic: increased size, increased echogenicity, accentuated corticomedulllary definition, and an RI of >0.75 |
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How do you treat acute tubular necrosis?
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- Correct the cause: improve perfusion to the kidneys and discontinue nephrotoxic drugs.
- Prevent and treat infections - If permanent kidney damage results, dialysis may be required. |
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What is acute cortical necrosis?
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A rare cause of acute renal failure caused by ischemic necrosis of cortex within sparing of the renal pyramids.
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What are the causes of acute cortical necrosis?
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- Sepsis
- Burns - Snake bites** - Pregnancy (placental abruption, septic abortion) |
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What are the clinical presentations of ACN?
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- Oliguria
- Hematuria - Flank Pain - Snake Bite - Severe trauma - Pregnancy (bleeding, abortion, and symptoms of eclampsia) |
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What are the sonographic features of acute cortical necrosis?
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Early:
- Renal cortex is hypo - normal-increased renal size Late: - increased cortical echogenicity - Cortical calcifications |
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How do you treat ACN?
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The damage is irreversible, patients with compromised kidney function require a low-potassium, low-phosphorus diet. The only option is dialysis leading to a kidney transplant.
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What is acute interstitial nephritis?
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Inflammation of the tissue surrounding the nephrons (interstitium).
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What are the causes of acute interstitial nephritis?
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Usually caused by an allergic reaction to antibiotic or antiinflammatory drugs:
- penicillin - ibuprofen - cyclosporine - sulpha May also result from infection. |
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Is AIN reversible?
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Yes if drug use is stopped
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What are the clinical presentations of AIN?
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- Recent history of infection or starting a new medication
- Fever - Rash - Generalized aches and pains |
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What are the SF of acute interstitial nephritis?
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Enlarged, echogenic kidneys
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What is chronic renal failure?
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A progressive loss of renal function due to gradual destruction of renal parenchyma.
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What are the stages of chronic renal failure?
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(1) Decreased renal reserve– patient asymptomatic
(2) Renal insufficiency – GFR is decreased – biochemistry starts to change (3) Frank renal failure – steadily increasing levels of protein end products (Creatinine, BUN) (4) Uremia – residual urine function is < 15%, biochemistry continues to elevate >> all body systems are impaired |
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What is glomerulonephritis?
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Inflammation and proliferation of glomerular tissue. Many causes and types (acute, chronic, post strep, etc). This is the leading cause of chronic renal failure in the US and Australia.
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What are the clinical presentations of glomerulonephritis?
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- Males **
- Ages 5-15* - Puffy eyelids, facial edema - Hypertension - Oliguria - Azotemia - recent infection (streptococcal) - hematuria - protein and RBCs in the urine |
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What are the SF of glomerulonephritis?
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Acute: normal enlarged kidneys
Chronic: Increased peripelvic fat, small echogenic kidneys. |
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How would you treat glomerulonephritis?
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- Prednisone
- Blood Thinners and antiinflammatories - Aggressive treatment of streptococcal infections - Dialysis - transplant |
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What does diabetes mellitus have to do with renal failure?
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It is the leading cause of chronic renal failure - hyperglycaemia causes hyper filtration and renal injury. There is an increased morbidity and mortality rate.
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What are the clinical presentations of diabetic nephropathy?
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- Diabetes for 10-20 years
- Foamy urine - Hypertension - Proteinuria - Diabetic retinopathy - Albuminuria |
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What are the sonographic features of diabetic nephropathy?
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- Enlarged kidneys
- With time: a decrease in size and an increase in cortical echogenicity - The pyramids have the same echogenicity as the cortex. |
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How would you treat diabetic nephropathy?
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- Insulin
- Anihypertensive medication - Dialysis -> Transplant |
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What are the cells of the liver?
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• Hepatocytes: the functional cell of the liver (synthesize, metabolize and excrete)
• Kupffer cells: fixed RE cells (remove and phagocytize old and defective blood cells,bacteria, & other foreign material) • Endothelial cells: compose the bile canaliculi and ductules |
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What are the functions of the liver?
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- Metabolism
- Storage - Secretion - Immunity - Vascular reservoir - Detoxification |
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Explain the metabolism function of the liver.
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• Hormones and drugs
• SYNTHESIZES:-proteins, glucose, clotting factors, (RBC’s in fetal life) • CONVERTS:-ammonia to urea -fatty acids to ketones -sugars to fats that can be stored |
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Explain the storage function of the liver.
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The liver stores vitamins and minerals and excess glucose as glycogen (released into circulation when blood glucose levels fall).
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Explain the secretion function of the liver.
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The liver secretes bile (h2O, bile salts, bilirubin, cholesterol, etc) and secretory proteins.
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What is the most important protein secreted by the liver?
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Albumin - controls osmosis
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Explain the immunity function of the liver.
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Filtration of blood and removal of bacteria and particles (actions of the kupfer cells).
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How much blood can the liver store?
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450 mL
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Explain the detoxification function of the liver.
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Breaks down poisons or transforms them into less toxic compounds. Phagocytosis of old WBCs and RBCs.
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What are some important biochemistry markers to watch for with liver pathology?
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- PTT (time required for a fibrin clot to form)
- Fibrinogen (plasma protein involved in clotting) - Bilirubin - Serum alkaline phosphatase (released by disorders affecting the bile duct) - Alkaline Aminotransferase (ALT - increased with liver injury) - Aspartate Amniotransferase (AST - increased with liver injury) - Albumin (low levels indicate hepatic disease) - Alpha Feto Protein (increased with HCC or presence of fetal tissue) |
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Which liver biochem marker is normally raised during pregnancy?
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Alpha feto protein
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What are the different types of bilirubin?
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Free - attached to albumin when transported in blood (increases with hepatic damage)
Conjugated - by hepatocytes making it soluble in bile (increased with biliary obstruction, no liver damage) |
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What is the alternate name for jaundice?
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Icterus
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What are the 4 major causes of jaundice?
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(1) Excessive destruction of RBCs (lots of hemoglobin breakdown)
(2) Impaired uptake of bilirubin by hepatocytes (3) Decreased conjugation of bilirubin (4) Obstruction of bile flow in lobules or bile ducts |
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What are the categories of jaundice causes?
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Prehepatic - excessive hemolysis of RBCs
Intrahepatic - m/c hepatitis and cirrhosis Posthepatic - obstruction between liver and intestine |
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Explain nuclear medicine studies.
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Tracer is the isotope that is to be uptake by a specific cell or tissue. A hotspot is an area of increased uptake and a cold spot is an area of decreased or no uptake.
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What are the 2 nuclear medicine tracers?
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(1) Gallium - uptaken by wandering RBCs, a positive exam is a hot spot (areas of infection, etc).
(2) TC- sulfur colloid - uptake by kupffer cells, a positive exam shows a cold spot where the tissue is damaged. |
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What are the clinical presentations of liver dysfunction?
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Jaundice, hemorrhage, acsites, hypoglycemia, encephalopathy, and infection
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What are the types of liver cysts?
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- true cysts (epithelial lining)
- peribiliary cysts - ADPKD - Biliary Harmatomas/ Von meyenburg complexes |
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What are true cysts?
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Fluid-filled space with an epithelial lining within the liver.
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What are the clinical presentations of true cysts?
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Asymptomatic- pain and fever (if infected or hemorrhagic)
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What are the SF of a true cyst?
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Anechoic*, thin wall*, posterior enhancement
- internal echoes and septations when infected |
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How would you treat a true cyst?
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Nothing , aspiration if becomes too large but a cyst with an epithelial lining will recur.
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What are the D/D for true cysts?
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A complex true cyst may be differentially diagnosed as cystic metastases. ADPKD is another D/D but for this you will see cysts in other locations.
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What are peribiliary cysts?
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Small, obstructed predicate glands located around the port hepatis (junction of hepatic ducts).
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What is the normal size of a peribiliary cyst?
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0.2-2.5 cm
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What is the clinical presentation of peribiliary cysts?
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Asymptomatic*, or biliary obstruction (depending on size)
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What are the SF of peribiliary cysts?
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Discrete, clustered, tubular appearing, thin septae, adjacent to the portal veins and bile ducts.
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What percent of ADPKD cases have associated liver cysts?
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57-74%
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How are the LFTs affected in ADPKD?
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They are not affected - primary kidney pathology
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What are the clinical presentations of ADPKD?
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- UTI
- Hematuria - High blood pressure - Kidney stones - Flank pain |
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How would you treat ADPKD?
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- Treat the symptoms (painkillers, lifestyle changes, etc)
- Transplant and dialysis is usually necessary |
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What are biliary hamartomas?
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Benign liver malformations, small - <1cm. They are composed of focal dilated intrahepatic bile ducts. They are often associated with congenital disorders like fibrosis and PKD
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What are the clinical presentations of biliary harmatomas?
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Asymptomatic
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What is the alternate name for biliary harmatomas?
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Von Meyenburg complexes
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What are the sonographic features of VMCs?
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- Well-defined, solid
- Uniformly hypoechoic - Bright echogenic foci with distal ringdown |
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What are the D/D for biliary harmatomas?
|
Lymphoma, hemangioma, or necrotizing entercolitis (air in portal venous system).
|
|
|
What is viral hepatitis?
|
Inflammatory process: diffuse swelling of the hepatocytes, proliferation of kupffer cells.
|
|
|
What are the different types of viral hepatitis?
|
A-E and G
|
|
|
What are the risk factors for carrier status?
|
- Impaired immunity
- Hemodialysis - Blood transfusions - Drug users - Sexual contact |
|
|
What is the difference between acute and chronic viral hepatitis?
|
Acute - leads to either complete recovery (within 4 months) or death, and is spread via the fecal-oral route.
Chronic - Inflammatory reaction of liver lasting more than 3-6 months with persistent abnormal biochem |
|
|
What can chronic viral hepatitis cause?
|
Portal hypertension, Cirrhosis, and HCC
|
|
|
What are the causes of chronic viral hepatitis?
|
HBV, HCV, HDV, autoimmune disease, drug induced, etc.
|
|
|
What are the clinical presentations of hepatitis?
|
- Fever
- Malaise - Nausea - Anorexia - Dark urine - Jaundice - RUQ tenderness |
|
|
What are the SF of acute hepatitis?
|
- Normal*
- Diffuse decrease in echogenicity - Bright portal triads (starry sky) - Periportal cuffing - Hepatomegaly - Thickened GB wall (edema) |
|
|
What are the SF of chronic hepatitis?
|
- Normal*
- Coarse echotechture and other morphological changes of cirrhosis |
|
|
What is the treatment of hepatitis?
|
Acute - Immune globulin
Chronic - Depends of specific aetiology, liver transplant Hepatitis C: interferon and ribavirin but there will be side effects |
|
|
What are the D/D of hepatitis?
|
Other causes (autoimmune, drug-induced, infectious).
|
|
|
How might someone contract pyogenic abscess?
|
- Direct extension from the biliary tracts in patients with suppurative cholangitis, or cholecystitis**
- Penetrating trauma - Enters the PV system due to appendicitis or diverticulitis |
|
|
What are the clinical presentations of pyogenic abscess in the liver?
|
- Fever
- Increased WBC count - Malaise - Anorexia - Jaundice |
|
|
What are the sonographic features of pyogenic abscess in the liver?
|
- Fluid-filled with posterior enhancement
- Pus: range of appearances from echofree to highly echogenic - Necrotic hepatocytes -> HYPOechoic - Fluid/fluid levels -> layering - Internal septations, debris - CLASSIC APPEARANCE = AIR |
|
|
How would you treat pyogenic abscess in the liver?
|
• Antibiotics
• Percutaneous Drainage • Surgery – last resort! If left untreated, 100% mortality. |
|
|
What are the D/D for pyogenic abscess of the liver?
|
- hematoma
- amebic abscess - necrotic cystic neoplasm |
|
|
What is Candidiasis?
|
Infection by the fungi of the genus candida. Part of the normal flora of the mouth, skin, intestinal tract and vagina.
|
|
|
What is the more well known name for candidiasis?
|
Thrush (throat mouth), yeast infection (vagina), cutaneous (skin) candidiasis.
|
|
|
How does candidiasis spread to other body systems?
|
Hematogenous spread of mycotic infection to solid organs.
|
|
|
Who will be affected by candidiasis?
|
Immunocompromised hosts: AIDS, cancer therapy, transplant patients.
|
|
|
What are the clinical presentations of candidiasis?
|
- Persistent fever in neuropenic patients
- Pain |
|
|
What will the biochem results of a candidiasis patient look like?
|
Candidiasis will be found in the blood
|
|
|
What is the treatment for candidiasis?
|
Antifungal drugs
|
|
|
What is the sonographic appearance of candidiasis?
|
There is a spectrum of appearances:
- Early: wheel within a wheel - Later: bulls eye (1-4cm, hyper echoic centre, with hypo rim) - Entire liver will appear uniformly hypo echoic, moth eaten appearance - in the chronic state it will look echogenic. |
|
|
What are the D/D for candidiasis?
|
- Mets
- Cirrhosis |
|
|
What is the most common opportunistic infection (in AIDS patients)?
|
Pneunocystis carinii (fungal infection)
|
|
|
What is the clinical presentation of patients with Pneunocystis carinii?
|
- CD4 cell count under 200
- Breathing difficulty - fever - Dry cough - Weight loss |
|
|
What are the SF of Pneunocystis carinii?
|
- Diffuse, tiny, non-shadowing echogenic foci
- Echogenic clumps - dense calcifications. |
|
|
What is the treatment for Pneunocystis carinii?
|
Antibiotics
|
|
|
What are the D/D for Pneunocystis carinii?
|
- M. avium-intracellulare complex
- CMV |
|
|
What is amebiasis?
|
It is an amebic abscess caused by entamoeba histolytica. It causes amebic dysentery (bloody diarrhea) and causes active necrosis of hepatocytes.
|
|
|
What are the clinical presentations of amebiasis?
|
- RUQ pain**
- Fever - Diarrhea - Hepatomegaly |
|
|
What is the biochem of a patient with amebiasis?
|
positive indirect hemagglutination test in 94-100% of patients
|
|
|
What are the SF for amebiasis?
|
Variable appearance:
- round/oval shaped lesion - absent abscess wall - Initially echogenic, laters uniform low-level echoes (hypoechoic due to necrosis of hepatocytes). - Posterior enhancement - within 4-8 weeks the necrotic tissue undergoes liquefaction and will have an anchovy paste appearance. - 8-12 weeks - complex appearance - 12+ weeks - predominantly echo-free pattern |
|
|
What is the treatment for amebiasis?
|
- Amebicidal drugs
- Aspiration (if not responding to meds) |
|
|
What is the mortality rate like for amebiasis?
|
If treated there is 10% mortality
If left untreated there is 100% mortality (as size increases rupture is imminent) |
|
|
What is the D/D for amebiasis?
|
Pyogenic abscess (you can tell the difference because amebiasis will have different blood work and dysentery)
|
|
|
What is hydatid Disease?
|
Tapeworm 3-6mm in length
|
|
|
What are the 3 layers of the cyst created by the hydatid tapeworm?
|
• Pericyst– Inflammatory response around cyst (made by host)
• Ectocyst – Outer layer (1mm thick; maycalcify) • Endocyst – Inner layer – ** daughter cysts develop fromgerminal epithelium - usuallywhen parent cyst has beenpresent approx. 6 months |
|
|
What are the CP of hydatid disease?
|
- Asymptomatic for 5-10 days
- Symptomatic when cyst is compromising another system (obstruction, pressure) - Fever and pain if infected - Anaphylaxis - rupture and leak of hydatid fluid |
|
|
What will the biochem for a person with hydatid disease look like?
|
CFT (complement fixation test)
|
|
|
What are the SF of hydatid disease?
|
(1) Simple cyst (no internal architecture except sand)
(2) Cyst with detached endocyst (waterlily appearance) (3) Cysts with daughter cysts (4) densely calcified masses |
|
|
What is the treatment of hydatid disease?
|
Percutaneous drainage, or surgery if too large - omentoplasty
|
|
|
What is schistosomiasis?
|
A common parasitic infection in humans causing chronic granulomatous disease
|
|
|
What is the other name for schistosomiasis?
|
Clay-pipestem fibrosis
|
|
|
What are the clinical presentations of schistosomiasis?
|
- Present with S&S of portal hypertension (splenomegaly, ascites, and varices) - fibrosis is compromisign lumen of portal vein
- Late presentation - Jaundice |
|
|
What are the SF of schistosomiasis?
|
- Widened echogenic portal tract up to 2cm (port hepatis*)
- Features of PH (early increased liver size, late decrease) |
|
|
What is the treatment for schistosomiasis?
|
Medicine
|
|
|
What is fatty liver's alternate name?
|
Steatosis
|
|
|
What is steatosis?
|
Response to trauma to the liver, an acquired, reversible disorder of metabolism. It is the accumulation of triglycerides in the hepatocytes.
|
|
|
What are the causes of fatty liver/steatosis?
|
- Obesity*
- Alcohol Abuse - Starvation - Cystic Fibrosis - Pregnancy - Type II Diabetes |
|
|
What are the clinical presentations of a fatty liver?
|
Asymptomatic
|
|
|
What will the biochem of a steatosis patient look like?
|
LFT's may be normal or mildly increased
|
|
|
What are the SF of focal fatty liver?
|
Infiltration (prone to earlyresolution - within 6 days!)
– *Segment 4 – Focal area of increased echogenicity Sparing – *GB fossa – Focal area of decreased echogenicity - Geometric margins present: well- defined - LACK OF MASS EFFECT (doesn't push or displace the hepatic veins) |
|
|
What are the SF of a diffuse fatty liver?
|
Mild: minimal increase of echogenicity, with normal diaphragm borders
Moderate: moderate increase in echogenicity, difficult vis of intrahepatic vessels and diaphragm Severe: marked increase in echogenicity, poor penetration, poor-no vis of diaphragm and IH vessels. |
|
|
How do you treat a fatty liver?
|
Remove the fatty stimulus
|
|
|
What are the D/D of a fatty liver?
|
- Mets (focal sparing)
- Hemangioma (focal fat) |
|
|
What is glycogen storage disease?
|
- An autosomal recessive disorder ofmetabolism - An enzyme deficiency leads to an error ineither the synthesis or degradation ofglycogen & subsequent use – large quantities of glycogen are stored in thehepatocytes and tubules of the kidney
|
|
|
What is the most common type of glycogen storage disease?
|
Von Gierke's (type I) disease is the most common type
|
|
|
What are the clinical presentations of glycogen storage disease?
|
(AR disorder - presents in childhood)
- Convusions - Lethargy - Nose Bleeds - Hepatomegaly |
|
|
What will the CP of glycogen storage disease be in the chronic stage?
|
- Cirrhosis
- Portal Hypertension - Renal Insufficiency |
|
|
What are the SF of glycogen storage disease?
|
- Hepatomegaly
- Diffuse increase in echogenicity - Some patients may develop HCC - Associated with hepatic adenomas |
|
|
How do you treat glycogen storage disease?
|
- Nasogastric feeding tube to sustain blood sugar levels
- Raw cornstarch diet - Surgical removal of adenomas |
|
|
What are the D/D of Glycogen storage disease?
|
This is indistinguishable from other types or causes of fatty infiltration.
|
|
|
What is liver cirrhosis?
|
Necrosis, Fibrosis, and Regeneration of liver tissue. Normal hepatocytes and kupffer cells are replaced by fibrous scar tissue causing liver failure. Vascular flow is disrupted and bile flow is also, causing portal hypertension and bile stasis.
|
|
|
Is liver Cirrhosis reversible?
|
No
|
|
|
What are the causes of cirrhosis?
|
– *Alcoholism
– * Viral Hepatitis – Cardiac disease – Hemochromatosis - Wilson’s disease - Primary Biliary Cirrhosis |
|
|
What are the CP of cirrhosis?
|
- It is a progressive disease that remains asymptomatic until the disease progresses too far
- It presents classically with hepatomegaly, jaundice, and ascites - Other symptoms: weight loss, weakness, S&S of portal hypertension |
|
|
What will the biochem of a patient with cirrhosis look like?
|
Abnormal LFTs
|
|
|
What are the SF of cirrhosis?
|
- early: increased echogenicity and size
- Late: increased echogenicity, and decreased size - Coarse echotexture - Nodular surface - Regenerating nodules will appear iso or hypo echoic - Dysplasic nodules will look premalignant |
|
|
What will cirrhosis look like under doppler?
|
Luminal narrowing of HV's with advanced disease with aliasing through.
|
|
|
How do you treat cirrhosis?
|
- There is irreversible damage here so you must treat the symptoms: increased carb and decreased protein intake, diuretics to decrease body fluids, and portocaval shunts.
- Liver Transplant |
|
|
What is portal Hypertension?
|
Increased pressure in the hepatoportalvenous system with a sustained pressure of >12mmHg
|
|
|
What are the casuses of portal hypertension?
|
Prehepatic: Extrahepatic, Presinusoidal, thrombosis of splenicand/or portal vein(s) (Trauma, sepsis,pancreatitis,splenectomy etc.), the liver is normal
Intrahepatic: Liver is abnormal – TRUE IH: *cirrhosis, diffuse mets, fibrosis, obstructinghepatic venous outflow (∴ increased HV pressure) – Presinusoidal: biliary cirrhosis, congential hepatic fibrosis, fibrosis in the portal zone (∴ N HV pressure) Posthepatic: Extrahepaticobstruction to portaloutflow (i.e. CHF, BuddChiari) liver is “congested” withblood |
|
|
What are the CP of Portal Hypertension?
|
- Ascites
- Splenomegaly - Varices - GI bleeding - Jaundice - Hepatic Failure - Hepatic encephalopathy |
|
|
What are the SF of portal hypertension?
|
- increased PV size (>13mm)
- Varices - Ascites - splenomegaly - Hepatofugal PV flow - Recanalized paraumbilical vein |
|
|
What are the treatment options for portal hypertension?
|
- Portosystemic shunts (spontaneous, surgical, TIPS)
- Transplant |
|
|
What are TIPS?
|
Transjugular Intrahepatic Portosystemic Shunts
- Stent serves as a low resistance pathway - We assess shunt patency at 3 points: HV end, PV end, mid (mean 135-200cm/sec) |
|
|
What are the complications of TIPS?
|
Stenosis and occulsion
|
|
|
What is Budd-Chiari Syndrome?
|
A rare condition that leads to cirrhosis and liver failure - occlusion of 1 or more HV with or without a blocked IVC.
|
|
|
What are the types of Budd-Chiari Syndrome?
|
Primary (congenital or web cord) and Secondary (tumour or thrombus)
|
|
|
What are the causes of Budd-Chiari Syndrome?
|
- Coagulation abnormalities
- Tumour extension - Trauma - Pregnancy - Oral Contraceptives |
|
|
What are the CP of Budd-Chiari Syndrome?
|
• In N. America:– Female young adult– On birth control pill– Acute onset of ascites, RUQ pain, hepatomegaly
• Asymptomatic – Long-standing disease ∴formation ofspontaneous redirection of blood;collateralization to capsular vessels |
|
|
What are the SF of Budd- Chiari Syndrome?
|
(1) Caudate lobe enlargement, decreased echogenicity
(2) Thickened walls, thrombosis, IH collaterals (3) Intraluminal echogenicity (4) Doppler: 3 hepatic veinsNOT seen (5) Ascites (6) Splenomegaly |
|
|
What are the treatment options for Budd-Chiari?
|
- Anticoagulants
- Thrombolytic therapy - Transplant |
|
|
What are cavernous hemangiomas?
|
- The most common benign tumour of the liver
- Hormone Dependent - Consists of many blood vessels intertwined with fibrous septa - Blood Pools - Peripherally in right lobe* - Solitary or multiple - No malignant potential |
|
|
What are the tests for hemangiomas?
|
- RBC scintigraphy***
- TSC -cold spot - CT - MRI - Ultrasound microbubbles |
|
|
What is the clinical presentation of a hemangioma?
|
- Women*
- Asymptomatic* - Pain with hemorrhage |
|
|
What are the SF of a hemangioma?
|
- Small (<3cm) - focal, well-defined, homogenous
- Hyperechoic* - Posterior Enhancement |
|
|
What are the Differential diagnoses for hemangioma?
|
- MCC
- Echogenic mets - focal fatty infiltration |
|
|
How are hemangioma's treated?
|
Small: no treatment, stop taking oral contraceptives
Large: Stop taking oral contraceptives, surgical removal |
|
|
What is focal nodular hyperplasia?
|
- 2nd most common benign liver mass
- Developmental HYPERplastic lesion - No risk of rupture or malignancy - Hormone dependent, NOT linked to oralcontraceptives |
|
|
What are the tests for focal nodular hyperplasia?
|
- TSC - hot spot
- Biopsy - Doppler: STELLATE VESSELS!! |
|
|
What is the clinical presentation of FNH?
|
Women in their childbearing years
- Asymptomatic |
|
|
What are the sonographic features of FNH?
|
- <5cm
- usually solitary - Central fibrous scar (hypoechoic)* - Subtle Contour Abnormalities |
|
|
How would you treat FNH?
|
- If large then remove surgically
- Get off any hormone pills |
|
|
What are the D/D of focal nodular hyperplasia?
|
- Adenoma
- Possible atypical hemangioma |
|
|
What are adenomas linked with?
|
Oral contraceptives
Von Gierke's disease (glycogen storage disease) |
|
|
Is there a malignant risk with adenomas?
|
Yes
|
|
|
What percent of adenomas rupture?
|
50%
|
|
|
What tests can be used to test for adenomas?
|
- TSC -cold spot
- CT - MRI |
|
|
What is the clinical presentation of adenomas?
|
- Women*
- Asymptomatic - RUQ palpable mass - Pain with bleeding or infarction - Shock (with tumour rupture) |
|
|
What are the SF of adenomas?
|
- Solitary, solid, vascular mass
- large >8cm - Variable echogenicity - Often composed of fat and/or calcifications which appear echogenic |
|
|
What are the D/D for Adenomas?
|
- HCC
- FNH - Hemangioma |
|
|
What is the treatment for adenomas?
|
- stop taking birth control
- Surgical resection |
|
|
Explain lipomas and angiomyolipomas.
|
They are rare tumours with no malignant potential. They are associated with renal AMLs and tuberous sclerosis.
|
|
|
What is the clinical presentation of lipomas and angiomyolipomas?
|
- Asymptomatic
|
|
|
What are the SF of lipomas and angiomyolipomas?
|
Solid, well-defined, echogenic tumours that have speed error artifacts.
|
|
|
What are some D/D for lipomas and AMLs?
|
- Hemangiomas
- Echogenic mets - Focal Fat |
|
|
What are the stages of malignancy?
|
Stage I - usually a tumor that can be completely removed withsurgery.
Stage II - usually a tumor that can mostly be removed by surgery butvery small amounts of the cancer are left in the liver. Stage III - usually a tumor that cannot be completely removed andthe cancer cells are found in the lymph nodes. Stage IV - cancer that has spread (metastasized) to other parts ofthe body. Recurrent - the disease has returned after it has been treated. Itmay come back in the liver or in another part of the body. |
|
|
What is HCC?
|
The most common primary malignant tumour of the liver.
|
|
|
What are the causes of HCC?
|
- Cirrhosis
- Hepatitis B and C - Aflatoxins (toxins produced by fungi) |
|
|
What are the 3 forms of HCC?
|
(1) Solitary
(2) Multiple (3) Diffuse |
|
|
How does HCC metastasize?
|
Venously through the PVs and HVs.
|
|
|
What is the clinical presentation of HCC?
|
- Men*
- Presents at advanced stage - Fever - RUQ mass - RUQ pain - Weight loss - Abdominal swelling |
|
|
What will the biochem of a patient with HCC look like?
|
Increased levels of AFP**
|
|
|
What are the SF of HCC?
|
- <5cm mass usually hypo echoic
- Hypoechoic halo - As size increases, homogeneity decreases - Lots of vascularity |
|
|
What are the D/D of HCC?
|
- Focal fatty sparing
- AML or lipoma - Hemangioma |
|
|
How would you treat HCC?
|
Depends on staging and patient condition
- Chemo - Alcohol or RF ablation if small and focal - Surgery |
|
|
What is fibrolemellar carcinoma?
|
A histologic subtype of HCC, but with a better prognosis
|
|
|
What is the clinical presentation of fibrolamellar carcinoma?
|
- Adolescents and young adults
- No Hx of liver disease - Palpable mass |
|
|
What will the biochem of a patient with fibrolamellar carcinoma be like?
|
Normal AFP because it is encapsulated (better prognosis)
|
|
|
What are the SF of Fibrolamellar carcinoma?
|
- Solitary
- 6-22cm - Variable echogenicity - Punctate calcs - Central echogenic scar |
|
|
What are the differences between HCC and fibrolamellar carcinoma?
|
HCC: presents commonly in males, with increased AFP, smaller tumours
Fibrolamellar Carcinoma: presents in adolescents with no hx of liver disease, and normal LFTs. Better prognosis, encapsulated and has calcifications and a central echogenic scar |
|
|
What is metastatic disease?
|
The neoplasm is secondary from the GB, colon, stomach, pancreas, breast, lungs, etc. Via blood-borne, lymphatics, or direct extension
|
|
|
What will the biochem look like for a patient with hepatic mets?
|
Increased SAP/ALP (serum alkaline phosphatase)
|
|
|
How would you treat liver mets?
|
Chemo and/or radiation therapy
|
|
|
What will the CP be for liver mets?
|
Extremely variable: hepatomegally, palpable mass, RUQ pain, Fullness, jaundice, and weight loss.
|
|
|
What are the SF of liver mets?
|
- multiple focal solid
- liver lesions - Hypoechoic halo - varying lesion sizes - GI tumour - hyper, lymphoma - hypo, lung tumour - bull's eye, breast and lung tumours have infiltrative patterns. |
|
|
What is hepatoblastoma?
|
The most common malignant liver tumour in children (most commonly in males <5)
|
|
|
What are the CP of hepatoblastoma?
|
- Failure to thrive
- Spiking Fevers - Anemia - Jaundice - Palpable mass |
|
|
What will the biochem of a patient with hepatoblastoma look like?
|
increased AFP
|
|
|
What are the SF of hepatoblastomas?
|
- Calcs present
- Usually solitary - Large - Mixed Echogenicity - Poorly marginated |
|
|
What is the treatment for hepatoblastoma?
|
Surgery, chemo, liver transplant, supportive care, antibiotics, follow-up care.
|
|
|
Where are trauma lesions most commonly imaged?
|
Right posterior segment
|
|
|
What is the modality of choice for trauma?
|
CT
|
|
|
What are the clinical presentations of trauma patients?
|
- may not present immediately
- Shock - Cold - Light-headed - External Injury - Pain |
|
|
What are the SF of trauma patients?
|
- Hemorrhage (varying appearances)
- Lacerations (hypoechoic line) |
|
|
What are the indications and contraindications of performing a biopsy?
|
Indications: For accurate diagnosis of focal lesions and diffuse liver diseases
Contraindications: Bleeding diathesis, unsafe route, or uncooperative patient. |
|
|
What is cholestasis?
|
Decreased bile flow through the canaliculi
|
|
|
What can cholestasis cause?
|
Unrelieved obstruction can cause fibrosis and ultimately biliary cirrhosis
|
|
|
What are the tests for biochem abnormalities of the GB?
|
- SAP
- Bilirubin - Biliary Scintigraphy (involves ionizing radiation) |
|
|
What is a normal GB wall thickness?
|
1-2mm in a fasting patient
up to 3mm in a non-fasting patient |
|
|
What might be the cause of luminal echoes in the GB?
|
- Stones
- Sludge - Pus - Blood - Tumour |
|
|
What is cholelithiasis?
|
The most common GB pathology caused by a build up of biliary substances (cholesterol and bilirubin) - could be due to abnormal bile composition, cholestasis, or GB inflammation.
|
|
|
What are the clinical presentations of cholelithiasis?
|
- Women*
- Asymptomatic - biliary colic - indigestion - Jaundice |
|
|
What are the risk factors of cholelithiasis?
|
Obesity, diabetes, increasing age, and pregnancy
|
|
|
How do you treat cholelithiasis?
|
Lithotripsy, or laparoscopic cholecystectomy.
|
|
|
What is the 4 F's?
|
It stands for Female, forty, fat, flatulent, and fair - risk factors for cholelithiasis.
|
|
|
What are the SF of cholelithiasis?
|
Echogenicity in the lumen with strong posterior shadowing. The stones should be assessed for mobility. There might be a WES complex,
|
|
|
What is a WES complex?
|
When the GB is totally filled with stones and the shadowing obliterates the lumen.
|
|
|
What are the D/D for cholelithiasis?
|
- porcelain GB
- GB polyps |
|
|
What is sand/sludge?
|
Thickened, concentrated bile
|
|
|
What are the contributing factors to sand/sludge production?
|
- Pregnancy
- Rapid Weight loss - Starvation - Critical illness - longterm TPN (total parenteral nutrition) |
|
|
What does sand and sludge increase the risk of?
|
Stone formation, acalculous cholecystitis, and pancreatitis.
|
|
|
What are the CP of sludge?
|
Asymptomatic
|
|
|
What are the SF of sludge?
|
- Low level echoes
- No acoustic shadow - Gravity Dependent - Mobile |
|
|
What are the D/D of Sludge?
|
- tumefactive sludge
- GB carcinoma |
|
|
How can the GB wall change?
|
- Wall thickening - focal (asymmetric), or diffuse (symmetric)
- Wall calcification - Adenomyomatosis |
|
|
What is the other name for a GB who's walls are calcified?
|
A porcelain gallbladder
|
|
|
How do GB walls calcify?
|
Rare, due to chronic inflammation and fibrosis. Fibrotic tissue is more prone to calcium deposits. Also associated with stones
|
|
|
What is there an increased risk of with a porcelain GB?
|
GB cancer
|
|
|
What are the CP of a porcelain GB?
|
Females*, 6th decade, asymptomatic, possible gallstone symptoms.
|
|
|
What are the SF of a porcelain GB?
|
- Hyperechoic semicircular line with dense posterior shadowing
|
|
|
What are the D/D for a porcelain GB?
|
- WES
- Emphysematous Cholecystitis |
|
|
What is adenomyomatosis?
|
A benign proliferation of smooth muscle and luminal epithelium. Invaginations of mucous epithelium into the muscle layer creates RA sinuses.
|
|
|
What does adenomyomatosis increase the risk of?
|
Cancer of the GB
|
|
|
Where is the most common location for adenomyomatosis (RA sinuses)?
|
Fundal region of the GB
|
|
|
What are the clinical presentations of adenomyomatosis of the GB?
|
Asymptomatic
|
|
|
What are the SF of adenomyomatosis?
|
- tiny echogenic foci with comet tail artifact (cholesterol crystals caught in the RA sinus)
- Focal mass-like area containing cystic spaces and echogenic foci with ringdown. - Can be in centre of GB causing an hourglass appearance or all the way around (looks like thickening of the wall) |
|
|
How would you treat adenomyomatosis?
|
Nothing
|
|
|
What are some causes of diffuse wall thickening?
|
- Acute cholecystitis (50-75%)
- Chronic cholecystitis (<25%) - Viral hepatitis - Hypoproteinemia (ascites) - Cirrhosis - CHF - AIDS (> 1 cm.) - Pancreatitis - Renal failure |
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What is acute cholecystitis?
|
Inflammation caused by chemical irritation from eh concentrated bile, >90% of cases result from gallstone obstructing the cystic duct/GB neck
|
|
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What is the etiology of acute cholecystitis?
|
Obstruction of cystic duct
> luminal distension, ischemia, superinfection > necrosis |
|
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What is the CP of acute cholecystitis?
|
- Women*
- <50 years* - Prolonged RUQ pain - Nausea - Vomiting - Increased WBC count - Fever |
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|
What will the biochem of an acute cholecystitis patient be?
|
Increased bilirubin and increased SAP
|
|
|
What tests are used to assess acute cholecystitis?
|
- Cholescintigraphy (demonstrates patency)
- CT |
|
|
What are the SF of acute cholecystitis?
|
Gallstones and a +murphy's sign is 92% predictive of acute cholecystitis.
- Thickened GB wall (>3mm) - Distended GB lumen (>4cm) - Pericholecystic fluid collections - Sludge - Hyperemic GB wall |
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What are the D/D for acute cholecystitis?
|
- Other pathologies that can demonstrate a positive murphy's sign and GB wall thickening: perforated duodenal ulcer, acute hepatitis, colitis, and diverticulitis
|
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How is acute cholecystitis treated?
|
Cholecystectomy
|
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What are the possible complications of acute cholecystitis?
|
- Gangrene
- Hemorrhage - Perforation - Bacterial Infection |
|
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What is gangrenous cholecystitis?
|
- Necrosis due to deficient or absent blood supply
- Up to 38% of pts with acute cholecystitis develop this - There is an increased risk of perforation (increased morbidity & mortality) - 50% of pts. develop generalized peritonitis |
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What complication can accompany gangrenous cholecystitis?
|
Hemorrhagic cholecystitis (bleeding within the GB wall)
|
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What are the CP of gangrenous cholecystitis?
|
- RUQ tenderness
- Positive murphy's sign (6% of cases) - Diffuse abdominal pain |
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|
What are the SF of gangrenous cholecystitis?
|
- Intraluminal membranes(sloughed membranes)
- Fibrous stranding - Irregular wall thickening - Collections within wall - Gas can be associatedwith gangrene |
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How is gangrenous cholecystitis treated?
|
It is a surgical emergency
|
|
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What is perforated cholecystitis?
|
- Occurs in 5-10% of pts. with prolongedinflammation (when cholecystitis is not treated)
- Mortality rate of up to 24% |
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|
What are the categories of perforated cholecystitis?
|
Subdivided into:
Acute – generalized peritonitis Subacute – pericholecystic abscess ** m/c Chronic – internal biliary fistula |
|
|
What is the CP of perforated cholecystitis?
|
Fever, chills, and pain
|
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What are the SF of perforated cholecystitis?
|
Primary sign: small defect in the GB wall
Secondary sign: deflated GB, fluid collection around the defect, and liver abscess |
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|
What is the treatment for a perforated cholecystitis case?
|
- Percutaneous drainage
- Surgery - Percutaneous cholecystostomy |
|
|
What is emphysematous cholecystitis?
|
A rare complication, gas producing bacteria has reached the injured GB after ischemia and chemical irritation via blood, lymph, or adjacent organs.
|
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What does emphysematous cholecystitis increase the risk of?
|
Increased risk of perforated and 15% of patients die.
|
|
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What are the CP of emphysematous cholecystitis?
|
- Men*
- 38% are diabetic - ⅓-½ have no gallstones - Vomiting - Jaundice |
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|
What is the treatment for emphysematous cholecystitis?
|
Urgent surgery
|
|
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What are the SF of emphysematous cholecystitis?
|
- Gas within wall &/orlumen
- Appears as non-dependent echogeniclines with posteriordirty shadowing orringdown artifact - Movement of gasbubbles - Pneumobilia |
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|
What is acute acalculous cholecystitis?
|
Inflammation of the GB in the absence of cholelithiasis - biliary stasis causes a change in bile constituents, which causes mucosal inflammation and release of enzymes.
|
|
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What are some risk factors for acute acalculous cholecystitis?
|
- Major surgery
- Severe Trauma - Sepsis - HIV - Atherosclerosis |
|
|
What can acute acalculous cholecystitis lead to?
|
Functional obstruction
- 52% lead to gangrene |
|
|
What are the CP of acute acalculous cholecystitis?
|
- Patients with severe underlying disease or prolonged critical illness
- Males* - Same S&S as acute cholecystitis (positive murphy's sign, pain, nausea, vomiting, increased WBC count, and fever. |
|
|
What are the SF of acute acalculous cholecystitis?
|
- Thickened GB wall
- Pericholecytic fluid - Intraluminal or intramural gas - Intraluminal membranes - Sludge/pus |
|
|
What is the treatment for acute acalculous cholecystitis?
|
Biliary aspiration (cholecystostomy)
|
|
|
What is chronic cholecystitis?
|
- Results from repeated bouts of the acute form
- Transient obstruction of the GB neck or cystic duct. - Chronic irritation of the GB by stones - Can lead to gangrene. |
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|
What are the CP of chronic cholecystitis?
|
- Intolerance to fattyfoods
- Occasional pain,discomfort - Belching, nausea - *Older women |
|
|
What are the SF for chronic cholecystitis?
|
- Thick Wall (in the absence of ascites, hypoalbuminea, CHF, non fasting)
- Cholelithiasis |
|
|
What is xanthogranulomatous cholecystitis?
|
Rare form of chronic cholecystitis, where lipid laden macrophages collect within the GB wall
|
|
|
What is the clinical presentation of xanthogranulomatous cholecystitis?
|
The same as chronic cholecystitis: intolerance to fatty foods, occasional pain, nausea, and belching.
|
|
|
What are the SF of xanthogranulomatous cholecystitis?
|
- Hypoechoic bands or nodules within a thickened GB wall.
|
|
|
What are cholesterol Polyps?
|
Polyps within the GB that can be focal (but multiple) or diffuse. They are benign and very common, not usually seen with stones.
|
|
|
What are the CP of cholesterol polyps?
|
- Asymptomatic
|
|
|
What is the alternate name for diffuse cholesterol polyps?
|
Strawberry GB (not seen sonographically)
|
|
|
What are the SF of cholesterol polyps?
|
- Multiple
- 2-10mm - non-shadowing oval lesions attached to the GB wall - Non-mobile - Don't change in size when followed |
|
|
What are GB adenomas?
|
- True Benign neoplasms of the GB
- Potential for malignancy but low - Single or multiple |
|
|
What are the SF of GB adenomas?
|
Hyperechoic (increased heterogeneity with increased size)
|
|
|
What is the D/D for GB adenomas?
|
- May be indistinguishable from GB polyps
|
|
|
What is the survival rate of GB carcinoma?
|
5- year survival rate of <5%
|
|
|
What are the 3 patterns of GB carcinomas?
|
- mass obliterating the GB
- Irregular wall thickening - Intraluminal polypoid mass |
|
|
What type of carcinoma makes up the majority of GB carcinomas?
|
98% are adenocarcinomas
|
|
|
What is the clinical presentation of GB carcinoma?
|
- Females
- >60 years of age CP resembles that of cholecystitis: jaundice, RUQ pain, fatty intolerance, and weight loss |
|
|
What are the SF of GB carcinoma?
|
- An abnormal appearing GB
- "trapped stone" sign (immobile stone trapped in tumour) - Malignant wall thickening - Polypoid mass (>1cm) |
|
|
Which types of cancers can metastasize to the GB?
|
- Melanoma
- HCC |
|
|
How would you treat GB carcinoma?
|
- Surgery (only considered unresectable if liver or peritoneal mets, exstensive nodal disease, or encasement of MPV or HA)
|
|
|
When can torsion occur with the GB?
|
Occurs in patients with a GB on a long suspensory mesentery.
|
|
|
What happens if the torsion is 180 degrees?
|
Gangrene
|
|
|
What are the CP of torsion?
|
Same as acute cholecystitis: RUQ pain, nausea, vomiting, fever, increased WBC count.
- Most common in elderly females |
|
|
What are the SF of a volvulus GB (torsion)?
|
Hugely distended and inflamed GB, GB is in an abnormal horizontal position.
|
|
|
What is the treatment for torsion of the GB?
|
Surgery
|
|
|
What is a fistula of the GB?
|
abnormal connection between (two hollow areas) gall bladder and any part of the bowel - associated with gall bladder perforation, from an increase on bile production.
|
|
|
What is gallstone ileus?
|
A mechanical obstruction caused bygallstone impaction in any part of the GItract – *distal ileum– Jejunum– stomach
- Usually occurs with stones >2.5cm |
|
|
What are the CP of gallstone ileus?
|
- >6th decade
- Progressive abdominalpain - Vomiting - Abdominal Distention |
|
|
What are the SF of gallstone ileus?
|
Rigler's Classic Triad
|
|
|
What is rigger's classic triad?
|
- Small bowel obstruction
- Pneumobilia - Ectopic gallstones |
|
|
How would you treat gallstone ileus?
|
- Surgery
- Depending on location - removal via colonoscopy |
|
|
What are hydrops? Causes?
|
A distended GB, caused by:
- Longstanding obstruction to the cystic duct or neck - Fasting - dehydration |
|
|
What is hydrops also known as?
|
Mucocele (accumulation of mucous)
|
|
|
What is the CP for Hydrops?
|
- Asymptomatic
- Chronic discomfort - RUQ palpable mass - RUQ pain |
|
|
What are the SF of hydrops?
|
- Distended GB
- Normal wall thickness - Possibly some sludge |
|
|
What is a courvoiser GB?
|
An enlarged, distended, palpable, non-tender GB
|
|
|
What is courvoisier GB caused by typically?
|
Obstruction to the CBD due to malignant neoplasm of the pancreatic head.
|
|
|
How will the GB change sonographically if the patient has undergone a cholecystectomy?
|
There will be no GB, the CBD will be dilated and the sphincters will regulate pressure.
|
|
|
Explain the types of biliary obstruction.
|
– intrapancreatic: dilatation of entire biliarytree
– suprapancreatic: dilatation of gb, proximal EH duct, IH ducts normal/small distal duct – porta hepatis: dilatation of right/left hepatic ducts, IH ducts – Intrahepatic |
|
|
What is the upper limit of normal for CBD size after a cholecystectomy?
|
10mm is the upper limit of normal
|
|
|
What is the most common cause of biliary obstruction? What is the most common level of obstruction?
|
Most common cause is choledocholithiasis, the most common level is intrapancreatic.
|
|
|
What is the clinical presentation of obstructive jaundice?
|
There is a sequence of events: (1) increased ALP
(2) Ducts dilate (3) increased bilirubin (conjugated) (4) pruritis (5) jaundice |
|
|
What are the two types of obstructive jaundice?
|
Painful: acute pain, stone*, infection
Painless: tumour* |
|
|
What are choledochal cysts?
|
Congenital cystic dilation of the biliary tree (focal or diffuse)
|
|
|
How many types of choledocal cysts are there?
|
5, type 1 is the most common (fusiform dilation of the CBD)
|
|
|
What do choledochal cysts increase the risk of?
|
cholangiocarcinoma
|
|
|
What is the treatment of choledochal cysts?
|
Surgical resection
|
|
|
What is the CP of choledochal cysts?
|
- Females*
- East asian population* - Asymptomatic - RUQ pain - Jaundice - Palpable Abdominal mass |
|
|
What tests can we run on choldochal cysts?
|
ERCP, MRCP, and biliary scintigraphy
|
|
|
What are the SF of choledochal cysts?
|
- Cystic structure around the port hepatis
- Communicates with the CBD - May contain sludge or stones |
|
|
What are the D/D for choledochal cysts?
|
pancreatic pseudocyst or enteric duplication cyst
|
|
|
What is carol's disease?
|
Rare congenital dilation of the IH biliary tree.
|
|
|
When will carol's disease occur?
|
Congenital hepatic Fibrosis
|
|
|
What is Caroli's disease associated with?
|
ARPKD and Medullary sponge kidneys
|
|
|
What are the 2 varieties of carol's disease?
|
- Simple/Classic
- Caroli's syndrome* |
|
|
What is the CP for carol's syndrome?
|
- patients are younger than 30
- Patients are vomiting blood (haematemesis) - S&S of PH: ascites, splenomegaly, varices |
|
|
What is the biochem like for caroli's syndrome?
|
Increased SAP and increased bilirubin
|
|
|
What are the SF of caroli's syndrome?
|
- Dilated IH ducts
- Stones/sludge within the ducts - Echogenic septae |
|
|
What are the types of choledocholithiasis?
|
Primary:
- Endemic in East Asia,otherwise RARE - Pigment stoneformation caused by: Caroli’s, Parasites, Sclerosing cholangitis, Chronic hemolyticdiseases Secondary: - Common - Migration of stones from GB - Found in up to 18% ofpts. with symptomaticgallstones - *distal duct @ ampullaof vater |
|
|
What is the CP for choledocholitiasis?
|
- RUQ pain
- Episodic jaundice - Asymptomatic - Nausea - Vomiting - Fever - Chills - Increased serum bilirubin |
|
|
What are the SF of Choledocholithiasis?
|
- Round echogenic mass with posterior shadowing
- If less than 5mm or a pigment stone - may not shadow - Linear echogenicities mirroring portal triads |
|
|
What are the D/D of choledocholithiasis?
|
- Hemobilia
- Cholangiocarcinoma |
|
|
How would you treat choledocholithiasis?
|
- Antibiotics to treat infection
- ERCP |
|
|
What is Mirizzi Syndrome?
|
Occurs in patients whose CHD and Cystic duct run in parallel, where a stone in the cystic duct is obstructing the CHD. This has an increased risk of fistula formation and a normal CBD.
|
|
|
What is the CP of mirizzi syndrome?
|
- Jaundice
- Fever - Pain |
|
|
What are the SF of mirizzi syndrome?
|
- Biliary dilation to level of CHD
- Acute/Chronic cholecystitis - Impacted stone in the cystic duct |
|
|
How would you treat mirizzi syndrome?
|
Surgery
|
|
|
What is pneumobilia?
|
Air within the biliary tree
|
|
|
What causes pneumobilia?
|
- Biliary intervention (stents)
- Acute cholecystitis (emphysematous and fistula) - Gallstone ileus |
|
|
What are the CP of pneumobilia?
|
S&S of the pathology causing the air
|
|
|
What are the SF of pneumobilia?
|
- non-dependent echogenic linear foci paralleling the portal triads
- Posterior dirty shadowing - mobile air bubbles |
|
|
What is hemobilia?
|
Blood in the Ducts
|
|
|
What are the causes of hemobilia?
|
- Trauma
- Cholangitis - Cholecystitis - Malignancy |
|
|
What are the CP of hemobilia?
|
Pain, bleeding, and biochemical jaundice
|
|
|
What are the SF of hemobilia?
|
- Blood clots areechogenic, mixedechogenicity
- Acute: low-levelechoes - Conforms to duct - Presence of blood in GB as well |
|
|
How would you treat hemobilia?
|
Treat the primary problem or let it resolve on its own.
|
|
|
What is ascariasis?
|
It is a Parasitic roundworm that uses the fecal-oral route of transmission.
- *children ages 2-10 - Seen in tropical countries with suboptimalsanitation practices – *Asia– Africa– South America - Worms can measure up to 30cm long! - Usually affects the EH ducts |
|
|
What are the CP of ascariasis?
|
- Asymptomatic
- Biliary colic - S&S of cholangitis, calculus cholecystitis, and pancreatitis |
|
|
What are the SF of ascariasis?
|
- A single worm* (echogenic tube, target appearance in transverse)
- Multiple worms (spagetti) - Look for worm movement |
|
|
What is clonorshis sinensis?
|
A liver fluke that lives in the biliary tree for 20-50 years. It mainly affects the IH ducts and has an increased risk of cholangiocarcinoma and cholangitis.
|
|
|
What is the definite host of clonorchis sinensis?
|
Humans
|
|
|
What are the clinical presentations of clonorchis sinensis?
|
- Asymptomatic - If more than 500 trematodes in the system: fever, chills, pain, and mild jaundice |
|
|
What are the SF of Clonorchis Sinensis?
|
- Dilated IH ducts
- Echogenicity &thickening of ductwalls - Flukes are notusually visible as: – 8-15mm in length– 1.5-5mm thick - Since it may causeRecurrent Pyogenic Cholangitis, it could havesimilar appearance |
|
|
What are fascilola hepatica?
|
Liver flukes that humans become infected through the consumption of contaminated veggies and water. The flukes measure 20-40mm in length.
|
|
|
What are the stages of infection through fascilola hepatica?
|
Acute (3-5 months) and Chronic (several years)
|
|
|
What is the CP for fascioliasis?
|
- Asymptomatic (chronic state)
- Acute RUQ pain - Prolonged fever - Hepatomegaly - Intraheppatic abscess |
|
|
What are the SF of fascioliasis?
|
- Variable
- Hypo/mixed echogenic lesions - Hilar lymphadenopathy - Hepatomegaly Sonography more useful in the chronic ductal phase: dilated ducts and flukes in the ducts/GB |
|
|
How do you treat parasites of the biliary system?
|
- Conservative therapy (anbithelminthics and antispasmodics)
- Surgery - Endoscopic intervention |
|
|
What are the 4 types of cholangitis?
|
(1) Sclerosing
(2) AIDs (3) Reccurent Pyogenic/Oriental cholangiohepatitis (4) Acute bacterial |
|
|
What is acute bacterial cholangitis?
|
Inflammation of the ducts by bacterial infection following biliary obstruction (85% associated with CBD stones, other causes: trauma, surgery, choledochal cysts)
|
|
|
What is the CP for bacterial cholangitis?
|
- Fever
- RUQ pain - Jaundice - increased WBCs - Increased SAP - Increased Bilirubin |
|
|
What are the SF of bacterial Cholangitis?
|
- Dilated bile ducts
- Choledocholithiasis - Sludge - Thick-walled bile ducts& GB - Possibility of liverabscesses |
|
|
How would you treat bacterial cholangitis?
|
- Antibiotics
- Decompression (aspiration) |
|
|
What is recurrent pyogenic cholangitis/oriental cholangiohepatitis?
|
- Chronic biliary obstruction, prolonged stasis
- Recurrent bouts of acute form - *Southeast and East Asians - Associated with Clonorchis sinensis in raw fish |
|
|
What are some possible complications of RPC/oriental cholangiohepatitis?
|
- Sepsis
- Segmental Atrophy - Liver Abscesses - IH biliary calculi - Biliary cirrhosis - Cholangiocarcinoma |
|
|
What is the CP of RPC/oriental cholangiohepatitis?
|
- Recurrent attacks of pain, fever, and jaundice
- Pinpoint pain with infectious abscesses |
|
|
What are the SF of RPC/oriental cholangiohepatitis?
|
- Most common in the ducts of the left lateral lobe
- Dilated ducts filled with sludge and stones (echogenic masses, heterogenous mass) |
|
|
What is the treatment of RPC/oriental cholangiohepatitis?
|
- Stone removal
- Liver resection - Drain the liver abscesses - Stents |
|
|
What is AIDS cholangitis?
|
Also known as HIV cholangiopathy, inflammation of the biliary tree in patients with advanced HIV infection
|
|
|
What is the CP of AIDS cholangitis?
|
Severe RUQ pain
|
|
|
What will the biochem of a patient with AIDS cholangitis look like?
|
CD4 count of <100 and increased SAP
|
|
|
What are the SF of AIDS cholangitis?
|
- Thickened IH & EH ductwalls
- Diffuse GB wall thickening - Thickened ampulla ofvater appears as anechogenic nodule in distalCBD - Focal strictures & dilationssimilar to PSC |
|
|
What is primary sclerosing Cholangitis?
|
- Chronic inflammatory condition of the biliary tree
- Destruction & fibrosis of the ducts which leads to: Biliary strictures, cholestasis, biliarycirrhosis, PH, Hepatic failure - Associated with inflammatory bowel disease(*ulcerative colitis) - Increased risk of cholangiocarcinoma - 10-15 yr. survival rate |
|
|
What are the CP of primary sclerosing Cholangitis?
|
- men around 40*
- Initially asymptomatic - Fatigue - Jaunice (if obstructing) - Bowel symtoms |
|
|
What are the SF of primary sclerosing cholangitis?
|
- Thick, irregular ductwalls
- Narrow lumen - Possibly some choledocholithiasis |
|
|
How would you treat primary sclerosing cholangitis?
|
Steroids or liver transplant
|
|
|
What is cholangiocarcinoma?
|
A rare neoplasm with risk factors like: primary sclerosing cholangitis, recurrent biliary infections and stones, and endemic populations of liver flukes.
|
|
|
What are the 3 types of cholangiocarcinomas?
|
- Klatskin's/Hilar*
- Distal - and Intrahepatic |
|
|
What is the survival rate of cholangiocarcinoma?
|
5-year survival rate of ~24%
|
|
|
What is the clinical presentation of cholangiocarcinoma?
|
- 8th decade
- Jaundice: – Dark yellow urine– Pale stools - Pruritis - Loss of appetite - Weight loss - Biochem: increased SAP and GGT |
|
|
What are the SF of an intrahepatic cholangiocarcinoma?
|
- *>1 polypoid masswithin IH bile duct
- Large, heterogeneous,HYPOvascular hepaticmass |
|
|
What are the SF of a distal cholangiocarcinoma?
|
- Duct-expanding polypoid lesion
- Irregular ductalconstriction - Duct wall thickening - HYPOechoic, HYPOvascular mass - Invasion into rest of ductalsystem & adjacentstructures |
|
|
Explain the position of Klatskin's tumour.
|
Usually the tumour will start in the right or left hepatic duct and extend into the higher order branches. There can be portal vein and nodal involvement and may metastasize to the liver and peritoneum
|
|
|
What are the SF of Klatskin's cholangiocarcinoma?
|
The Classic appearance: dilated IH ducts, and the right and left hepatic bile ducts do not unite.
|
|
|
How would you treat cholangiocarcinoma?
|
- Depends on location, size, patient condition, andevidence of spread
- DistalForm: Whipple’s Procedure/Pancreaticoduodenectomy - Klatskin’s: Extended lobectomy, unresectable if: encasing, narrowing, or obliteratingthe MPV or HAP - For Unresectable Tumours: treat symptoms,palliative – Stent insertion– Chemotherapy |
