4_primer_mankad_hoey_20150316195755 Flashcards
Renal Embryology
Kidneys form from pro-, meso- and metanephros; first two regress and only latter persistsUreteric bud from outgrowth of mesonephric ductForm in sacrum and migrate caudally by 8 weeks gestation; maturation continues to 5 y/o
US Medulla Cortex
Renal medulla hypoechoic to cortex
Renal Mass CT protocol
NoncontrastCorticomedullary phase (25-30 seconds)Nephrographic phase (80 seconds)
Location Septum of Bertin
90% upper pole, 60% bilateral Associated with bifid renal pelvis
Congenital megacalyces
Excess of enlarged calyces (20-25 vs normal 10-14), causing hypoplastic pyramidsNo obstruction, normal renal parenchyma and function
Pyelocalcyceal Diverticulum Types
Outpouching of calyx into corticomedullary region; usually asyptomatic but may cause calculiType 1: from minor calyxType 2: from infundibulumType 3: from renal pelvis
ADPKD
Cystic dilatation of collecting tubules and nephrons; 0.1% population, 10% dialysis patients, strong penetranceHepatic cysts (70%), intracranial berry aneurysms (20%), pancreatic and splenic cysts 60 y/o
Acquired cystic kidney disease
Multiple renal cysts developed in CRF; occur in 90% patients on dialysis3-5 cysts in each kidney, CRF and no history of inherited cystic diseaseHemorrhagic cysts occur in 50%, can ruptureRCC develops in 7%
Bosniak criteria
- Benign simple cyst, don’t communicate with collecting system2. Minimally complicated, benign but with concerning featuresThin septations (20) 2F. Multiple septa with or without perceptible but not measurable enhancement; can have thick or nodular calcification, also included if hyperattenuating and >3 cm3. Complicated, multiloculated but with malignant features. 4. Clearly malignant with large cystic component
Medullary cystic disease
Due to tubulointerstitial fibrosisPresents with anaemia and renal failureSmall kidneys with multiple small medullary cysts, often merely causes medullary increased echogenicity, thinned cortexThree typesFamilial nephronophthisis (70%): AR, juvenile onset at 3-5 years but also adult typeAdult medullary cystic disease (15%): AD inheritanceRenal retinal dysplasia (15%): recessive, associated with retinitis pigmentosa
Causes of Nephrocalcinosis
Metastatic (normal kidneys), dystrophic (injured tissue) or urine stasisHyperparathyroidism (primary and secondary)Metastatic carcinoma to bone and hypercalcaemia of malignancyProlonged immobilisationSarcoidosisMilk alkali syndromeHypervitaminosis DRTA (often dense medullary calcification)Medullary sponge kidney (urine stasis)HyperoxaluriaBartter’s syndromeProlonged frusemide (usually premature infants)Nephrotoxic drugsPapillary necrosis
Medullary sponge kidney
AKA Benign renal tubular ectasia, Cacchi-Ricci diseaseDysplastic cystic dilatation of papillary / medullary portions of collecting ducts, usually 20-40 y/o75% bilateral, often asymptomatic; 10% develop progressive renal failureIVP - striated nephrogram (brushlike), ‘bunch of flowers’ appearanceAssociations: Hemihypertrophy, Beckwith-Wiedemann, Pyloric stenosis, Ehlers Danlos, RTA, any form of renal cystic disease / ectopia,
RCC Types
Best evaluated in nephrographic phase, venous invasion best characterised by MRIUS: 70% hyperechoic if > 3 cm, 30% if
Oncocytoma
From epithelial cells of proximal tubule, usually well-differentiated and benign but need resectionCentral stellate scar (25-33% on CT) and spoke wheel (angiography), usually homogeneous enhancement, can’t differentiate from RCC on imaging, but FNA can discriminate
Staging RCC
I: kidney onlyII: extrarenal ± adrenal involvement, but confined within Gerota’s fasciaIII: A - renal vein, B - lymph node metastases, C - bothIV: A - direct extension to other organs through Gerota’s fascia; B - metastases (lung (55%) > liver > bone > adrenal > contralateral kidney (10%))
Renal lymphoma
Occurs in 8% lymphoma patients, 75% bilateral, NHL > HL.Characteristically, renal vessels remain patent despite encasementMR: hypointense to cortex on T1W, heterogeneously hypo to isointense on T2WPatterns (five):Mulitple renal masses (59%)Solitary mass (3%)Renal invasion (contiguous RP spread)Perirenal (10%)Diffuse renal infiltration (rare)
Renal metastases
Fifth most common metastatic site, mainly haematogenous spreadLung, breast and contralateral kidneyColonic metastases often solitary and exophyticMelanoma metastases often have perinephric extension
Angiomyolipoma
Benign hamartomas - blood vessels, smooth muscle, fat; DO NOT contain calcificationCan cause pain, haematuria, anaemiaUsually multiple in tuberous sclerosis (80% of TS have AML)Sporadic form commonest (80-90%): F/M = 4/1, usually middle aged; thus 4 cm often resected / ablated.Intratumoural fat almost diagnostic (CT or chemical shift), 5% do not contain fatMay extend into renal vein and IVC
Tuberous sclerosis
AD, variable penetrance; >50% sporadicEpilepsy, mental retardation and adenoma sebaceumAlso subependymal nodules, giant cell astrocytoma, peripheral tubers, retinal hamartomas, cardiac rhabdomyomas, lymphangioleiomyomatosis, shagreen patches, subungual fibromas, bone cysts50% have renal lesionsBilateral renal cystsMultiple AMLs are sine qua non of TS (15% patients)RCC (1-2%)
Renal adenoma
Solid lesion
Renal Pelvis Tumours
Tend to maintain reniform outline of kidneyInverted Papilloma (No malignant potential, 20% risk of associated urothelial malignancy)TCCSCC (5% renal pelvis tumours,
TCC of Upper Renal Tract
Often multifocal; 40-80% have bladder TCC but only 3% bladder TCC later develop upper renal tract TCC10% of upper renal tract neoplasms, 2-4% bilateral, 2-7% calcificationHyperechoic on US and hyperattenuating on CTCauses faceless kidney - obliteration of sinus fat and infiltration of parenchymaStippling sign on IVP - tracking of contrast interstitially in papillary lesionStricturing - thus can mimic renal TB60% ipsilateral recurrence and 50% have lung metastasesStage I and II: limited to lamina propria / muscular layer, III: renal parenchyma / adjacent fat, IV: metastatic (usually liver, lung, bones)
Indications for partial nephrectomy
Solitary RCC
Von Hippel Lindau
AD, almost 100% penetranceUsually renal cysts25-40% develop clear cell RCC (often 30-40 y/o), often synchronous / metachronous; often screen from 20’s.Also have pancreatic cysts (30%), islet cell tumours, phaeochromocytomas (10%, often multiple and ectopic, 50-80% bilateral), retinal angiomas, ANS haemangioblastomasMore rarely endolymphatic sac tumours, cystadenomas of epididymis, broad ligament cysts
GU Tuberculosis
Second most common site of TB, usually haematogenous spread, may be asymptomaticActive / healed pulmonary TB in 50%50% calcification (amorphous granular if active, dense punctate if healed tuberculomas - putty kidney)Usually bilateral asymmetrical involvement, 25% unilateralTubercles become cavities, communicating with calyces, which then stricture, can cause autonephrectomyCan cause epididymitis, hydrocoele, testicular mass, prostatitis, female infertility
GU Tuberculosis Imaging features
Kidneys - Smudged papillae, moth-eaten calyx, ‘hiked-up’ pelvis - cephalad retraction of infero-medial margin of pelvis at PUJUreters - Usually unilateral, beaded corkscrew appearance (alternating scarring & dilatation), aperistaltic and shortened (pipestem)Bladder - Chronic interstitial cystitis causing fibrosis; Small, trabeculated, VU reflux, wall rarely calcifiedProstate - Dense calcification
Emphysematous pyelonephritis
Usually diabetic & E Coli (gas forming gram negatives) infection, occasionally non-DM with obstructionBest diagnosed on CT, often requires nephrectomy if severeType 1 (pyelonephritis): Destruction > one third renal parenchyma, 70% mortality, gas in parenchymaType 2 (pyelitis): Destruction
Xanthogranulomatous pyelonephritis
Replacement of renal parenchyma by lipid laden macrophages, begins in pelvis and extends to cortex and medullaMultiple low attenuation (-10 to 30 HU) xanthomatous masses (may show fine calcifications, thin rim of peripheral enhancement) ± thickened Gerota’s fascia ± psoas abscessChronic indolent bacterial infection, usually E Coli or Proteus; 10% diabetic, typically middle aged females90% diffuse, 10% focalAbsent / decreased contrast excretion on affected side75% due to staghorn calculus; 25% due to PUJ obstruction or tumourMay lead to replacement lipomatosis (severe parenchymal atrophy)
Renal papillary necrosis and causes
Ischaemic coagulative necrosis of pyramids / medullary papillae; chronic tubulointerstitial nephropathy; predominantly affects medullaGradual development of cleft in papilla ± sloughing ± rimlike calcification’Lobster claw’ initially, then ‘ring sign’ around sequestered sloughed papilla, ultimately calyceal blunting after necrosis and absorptionCauses (due to ischaemic and/or infective necrosis)DMAnalgesiaSickle cellPyelonephritisRenal vein thrombosisTuberculosisObstructive uropathy
Renal Trauma Categories
80% blunt trauma, 20% penetratingAbsence of haematuria does not preclude serious renal injuryI (75-85%): Contusions, small lacerations with no communication with collecting system (includes isolated subcapsular and perinephric haematomas, conservative managementII (10%): Laceration through cortex ± urine extravasation; may be managed conservativelyIII (5%): Multiple deep lacerations with renal pedicle injuryIV (rare): PUJ avulsion / laceration of renal pelvis
Renal Haemorrhage
Suburothelial - thickened wall of pelvis / proximal ureter due to bloodSubcapsular - recent blood is higher attenuation than parenchyma, kidney flattened with elevated capsule, eventually may calcify; if large and chronic may cause hypertension (Page kidney)Perinephric - usually extends below renal margin
Renal infarction
Due to RA thrombosis or embolism, vasculitis, trauma, sickle cell, aortic dissectionRenal Artery Occulsion may present with Severe flank pain, haematuria, albuminuria, leukocytosis, fever, tender renal mass; or may be asymptomaticTypesGlobal: Non-enhancing kidney, high density capsular rim (collateral perfusion)Large branch occlusion: Wedge shaped defect, base on capsule, apex towards hilum, ± cortical rim enhancementSmall vessel occlusion (emboli, vasculitis, sickle cell): Multiple, often bilateral infarcts, ‘slit-like’ in sickle cell, may show cortical rim enhancement (unlike pyelonephritis)
Renal vein thrombosis
Causes smooth, swollen kidney with variable contrast excretion (can be dense nephrogram) ± occluded collecting systemCan cause cortical rim sign; varices may indent pelvis / ureterCT: prolonged corticomedullary differentiation, characteristic fine linear densities extending from kidney to perirenal space, enhance post contrastUS: Initially hypoechoic, then hyperechoic at 10 days due to cellular infiltrates / fibrosis; in late phase (several weeks) small hyperechoic kidney with loss of corticomedullary differentiationIf complete acute occlusion, can cause infarctionCauses:Malignant (extrinsic compression or direct extension)Primary renal disease (membranous GN commonest, SLE, amyloid)Secondary from IVC thrombosisInfants: sickle cell, haemoconcentration (diarrhoea, sepsis), hypoxia in congenital heart disease, maternal diabetes
Acute Cortical Necrosis Definition, Causes
Pathological progression of ATN; Ischaemic cortical necrosis with medullary sparing; usually bilateralAcute: unenhanced cortex between enhancing medulla and enhancing cortical rimChronic: small smooth kidneys, may show cortical calcificationCauses (60% ischaemia, 40% nephrotoxins): Haemorrhage (classically 3rd trimester)Septic abortionTrauma with shockSevere dehydrationHaemolytic uraemic syndromeAcute aortic dissectionTransfusion reactionToxins (including snake venom)
Renal artery stenosis
Causes: atherosclerosis (90%; narrows ostium or proximal 2 cm of RA), FMD (mid-distal RA, ‘string of beads’)Causes 1-5% HTN in young adultsCECT: Prolonged CMD implies significant stenosisCEMRA: Highly sensitive in proximal RASAngiography: Gold standard, but can’t assess haemodynamic significance of lesionUS: Peak systolic velocity > 150 cm/s, acceleration time > 0.07 s (parvus et tardus waveform), post-stenotic spectral broadening / flow reversal
Renal Transplant Complications
ATN (normal flow, reduced excretion) - rarely occurs > 1 month post transplantRejection (Resistive index >0.7 ([systolic-diastolic]/systolic, nonspecific), 90% show increased size (but normally decreased if chronic); thickened cortex; large renal pyramids with indistinct CM junction, focal hypechoic areas in cortex / medulla (20%), increased cortical echogenicity (15%)); hyperacute rejection shows decreased flow but delayed excretionCyclosporine toxicity - similar pattern to ATN but later post-transplant, rare within first monthArterial occlusion (87% success of angioplasty for anastomotic stenosis)Venous occlusion (RVT normally occurs in first 3 days post transplant)Urinary leakUrinary obstruction
Causes of perirenal fluid collections post-transplant
Lymphocoele (10-20% at 1-4 months post transplant; usually inferomedial to kidney and linear septations present in 80%)Abscess (usually develops within weeks)Urinoma (develops in first month, generally near VUJ, may be cold on nuclear medicine if not active)Haematoma
Ureteric development
From ureteric bud (if >1 bud, can have ureteric duplication), arising from mesonephric duct; 10-25 calyces/kidneyWeigert-Meyer: Upper moiety ureter inserts inferomedial to lower moietyThus upper moiety can develop ureterocoele (cobra head on IVP; can project into bladder and obstruct other ureter), lower moiety develops refluxUpper moiety may have extravesical insertion - typically bladder neck, urethra or vagina / seminal vesicles, vas deferensEctopic ureter F/M = 6/1; causes UTIs, obstruction, incontinence
Retrocaval ureter
Ureter passes behind IVC and exits between aorta and IVCMedial looping at L2/L3 on IVP, can cause ureteral narrowing
Ovarian vein syndrome
Right gonadal vein crosses ureter and drains into IVC, left gonadal vein drains to left renal veinUreteral notching / dilatation / obstruction due to ovarian vein thrombosis / varicesAssociated with pregnancy
Retroperitoneal fibrosis
Idiopathic form (two thirds) = Ormond’s Disease (M>F)Originates just inferolateral to aortic bifurcation and extends superiorly, but limited anteriorly by peritoneumTypically involves left ureter before right, usually at L3-L5 levelAssociations - IBD, PSC, fibrosing mediastinitis, Riedel’s thyroiditis, sclerosing mesenteritis, orbital pseudotumourImaging - Soft tissue layered around aorta and IVC, loss of peristalsis in involved ureteric segment (but always spares ureteric mucosa), does not extend between aorta and vertebrae (unlike malignant lymphadenopathy)Early or malignant RPF - high T2W; mature fibrotic plaque - low T2WRenal impairment out of proportion with degree of hydronephrosis, but stenting usually easy
Causes and Sequelae of RPF
Causes:AAARP metastases (lymphoma, breast, carcinoid) - Desmoplastic reaction: HD > NHL > anaplastic & metastasesRP haematomaRP abscess (diverticular, appendix)UrinomaDrugs (hydralazine, methylsergide, methyldopa, ergot)RadiationSequelae:Lower extremity / scrotal oedemaDVT
Retroperitoneal tumours
90 % malignant, usually > 10 cm at diagnosisMesodermalLiposarcoma (usually myxoid or pleomorphic; little fat on CT)Leiomyosarcoma (large heterogenously enhancing mass, central necrosis)FibrosarcomaLymphoma, othersNeuralNeurofibromaNeuroblastomaPhaeochromocytomaEmbryonicTeratomaPrimary germ cell tumour
Pelvic lipomatosis
True pelvis infiltrated by unencapsulated mature adipose tissueTwo thirds of cases are black malesCauses UTIs / obstruction, constipationAssociations: cystitis glandularis (75%, form of proliferative cystitis), increased risk bladder adenocarcinoma’Inverted pear’ shaped bladder, reduced bladder capacity, medial deviation of uretersEnlarged retrorectal space on Ba enema
Ureteritis cystica
Sterile submucosal fluid collections due to intramural inflammation, causing encystment and submucosal extension of transitional epithelium; not premalignantUsually unilateral, multicentric, smooth, round filling defects on IVU (most 2-4 mm diameter)Associated with chronic UTIs
Ureteral Psuedodiverticulosis
Outpouchings 1-2 mm of epithelium into lamina propria, associated with inflammation50% develop uroepithelial malignancy
Ureteric trauma
Usually penetrating injury causing urinoma / discontinuity / extravasationAvulsion usually at PUJ due to deceleration (commonest in children)
Malakoplakia
Yellow subepithelial plaques of mononuclear histiocytes containing Michaelis-Gutmann bodiesCobblestone appearance on IVP, most common in bladderF>M, usually diabetic or immunocompromised, strong association with E Coli UTIsCauses LUTs and haematuria; rarely invades bone
Ureteric tumours
50% develop bladder cancer, 75% unilateral, 5% bladder cancer patients develop ureteric cancerMalignant: Epithelial - TCC, SCC, adenocarcinoma; Mesodermal - Sarcoma, angiosarcoma, carcinosarcomaBenign:Epithelial - inverted papilloma, polyp, adenomaMesodermal - fibroma, haemoangioma, myoma, lymphangiomaGoblet sign: retrograde pyelogram with dilated ureteral segment distal to obstruction, with filling defect and mensicusMetastatic sites of ureteric primaries: RP LNs (75%) > liver, lung (60%) > bone (40%) > GIT (20%)
Bacterial cystitis
E Coli > Staph > Strep > PsuedomonasMucosal thickening (cobblestone), stranding perivesical fatEmphysematous cystitis usually E Coli in DM, neurogenic bladder (S2-S4 dermatome; UMN lesion = spastic, LMN lesion = atonic) or outlet obstruction (intramural gas, air/fluid level in bladder)
Cystitis cystica and glandularis
Cystica - mulitple serous fluid filled cystsGlandularis - mucin-secreting glandular hypertrophyChronic reactive inflammation, causes LUTs; muscle layer is intact; both can coexist with GU TBFilling defects on urography with hypervascular polypoid mass on CT & MRLow T1W, low signal with central branching high signal on T2W
Miscellaneous causes of cystitis
Radiation: approximately 15% of patients receiving pelvic irradiationCyclophosphamide: 40% develop haemorrhagic cystitisEosinophilic: Allergic reactions
Schistosomiasis
Association with bladder SCC, foreign body reaction in mucosa, M>F. DDx = TBBladder becomes fibrotic but remains distensible and normal volume.Inflammatory pseudopolyps = bilharzomasXR: Bladder wall (initally anterior at base, then encircles) and distal ureteric calcification (parallel / linear)IVU: Ureteritis cystica, ureteric dilatation / strictures
Inflammatory pseudotumour
Non-neoplastic proliferation of myofibroblastic spindle cells and inflammatory cells with myxoid componentsSymptoms: Haematuria, iron deficiency anaemia, feverSingle exophytic / polypoid bladder mass ± ulceration (but solid and cystic variants); spares trigone, can extend extravesicallyEnhances post contrast on CT and MR, can have internal flow on US
Endometriosis
Bladder commonest site of urinary tract involvement (1-5% of endometriosis, premenopausal only), cyclic haematuria in 20%Usually posterior wall above trigone or dome, may be inseparable from anterior wall of uterus, tends to be deeply infiltratingHigh signal T1W ± high signal T2W ± homogeneous or peripheral contrast enhancement
Nephrogenic adenoma
Benign reactive process to chronic irritation involving lamina propria but not muscle, not premalignant63% recurrence post resection
Bladder malignancy
4% of all cancers, M/F = 3/1, 50-60 y/oTCC (90%) - aniline dye, phenacetin, radiation, tobacco, interstitial nephritisSCC (5%) - calculi, chronic infection, schistosomiasisAdenocarcinoma (2%) - bladder exstrophy, urachal remnant, cystitis glandularis (10% pass mucus PU)95% carcinomas; leiomyosarcoma is commonest non-epithelial malignancyMetastases to bladder: stomach, breastUrachal carcinoma (0.4% bladder cancer, 40% bladder adenocarcinomas) - 70% calcified, 70% occur before 20 y/o
Staging bladder cancer
T1: Mucosa and submucosaT2: Superficial muscle layerT3a: Deep muscle layerT3b: perivesical fatT4: other organs
Leukoplakia
Squamous metaplasia of transitional epithelium (keratinisation), uncertain if premalignant; 30% have haematuriaAssociations: chronic infection (80%), calculi (40%)
Bladder trauma
Extraperitoneal rupture (Pelvic fractures) - conservative managementUsually occurs anterolateral at bladder baseCauses pear shaped bladderIntraperitoneal rupture (Blunt trauma, stab wounds) - surgical treatmentUsually occurs bladder domeContrast collects in paracolic gutters
Urethral injuries
Type 1: Intact urethra, stretched and narrowed by periurethral haematomaType 2: Rupture above urogenital diaphragm; extraperitoneal contrastType 3: Rupture below urogenital diaphragm; contrast in extraperitoneal space and perineum
Urethral strictures - causes
Gonococcal (commonest in USA, 40%) - usually bulbopenile urethraTB - ‘watering can’ perimeumCondylomata acuminata - HPV infection, papillary filling defectsTrauma - instrumentation, catheters (usually penoscrotal junction)Tumors (SCC 80%, TCC 15%; prostate cancer)
Female urethra, diverticulum and carcinoma
Female urethra ≤ 4 cm longDiverticula usually due to obstruction of Skene’s glandsCarcinoma - F/M = 5/1, 70% SCC, 90% in distal two thirds
Vas deferens course
Posterior aspect spermatic cord, diverges at deep inguinal ring, passing anterior to internal iliac artery, forming ejaculatory duct with seminal vesicle at prostatic base
Contents of Spermatic cord
vas deferens, vessels, lymphatics (drain to lateral and preaortic nodes) and nervesNeurovascular bundle in spermatic cord:Internal spermatic (tesicular - aorta), external spermatic (cremasteric - inferior epigastric) and differential arteries (to epididymis and vas - vesicular branch of internal iliac)Pampiniform plexus drains to ipsilateral testicular veinNerves: cremasteric nerve, genital branch of genitofemoral nerve and testicular sympathetic plexus
Testicular embryology
Genital ridges extend from T6 to S2Mesenchyme between seminferous tubules forms Leydig cells (begin to secrete testosterone at 8 weeks)Mesonephric ducts form epididymis, vas deferens, seminal vesicles and ejaculatory ducts, while paramesonephric ducts regressAt 7-8 weeks, testes descend to pelvis, staying at deep inguinal ring until seventh month, then descend to scrotum
Epididymitis
Commonest postpuertal acute scrotal pathology, likely ascending infection (gonococcal, E Coli, pseudomonas, TB); 20% develop orchitisAcute US: Swollen hyperaemic (only sign in 20%) hypoechoic epididymis (>5 mm thick)Thickened scrotal skin ± hydrocoele (if complex suggests pyocoele)Chronic US: Swollen epididymis ± hyperechoic
Orchitis
Commonest complication of mumps infection in postpubertal males (in which case usually unilateral); causes unilateral atrophy in one third, bilateral in 10%; atrophy detectable by 6 monthsUS: Enlarged, hypoechoic (usually), hyperaemic testisFocal orchitis does not distort testicular contour (unlike cancer)
Varicocoele
L (95%) > R, 25% bilateral; if solitary on right - concern for RP malignancyAbnormal dilatation pampiniform plexus, causing compressible scrotal veins > 2 mm diameter, more prominent on valsalva or standing
Testicular Ca types
Germ cell [SpECT] (95%; metastases may have different histology from original tumour):Seminomas (40%) - do not cause elevated AFP; homogenously hypoechoic, usually focal but may be diffuse, sharp interface with normal parenchyma; radiosensitiveMixed (40%) - teratocarcinoma is commonestNon-seminomatous GCT (more aggressive)Embryonal Cell Carcinoma (10%) - cystic, heterogenous, ‘wild’Teratoma (10%)Choriocarcinoma (1%, aggressive, early haematogenous metastasis, frequently to brain)Yolk sac carcinomaNon-germ cell (5%; ‘sex cord’; usually benign)Leydig cell (can produce testosterone, 30% cause virilisation / feminisation)Sertoli cell (can produce oestrogen and present with gynaecomastia)Lymphoma (most common tumour in older men, may be bilateral) - less distinct marginMetastasesProstate, lung, kidney, GIT, myeloma, leukaemia
Testicular Ca lymph nodes
Sentinel LNsLeft - left renal perihilar group (just below left renal vein)Right - paracaval LNs at or below right renal veinHaematogenous spread is most commonly to lungs; then liver, bone and brain
Testicular Ca Staging
Low: confined to testis / epididymis / spermatic cord (T1-3), mild / moderate LNs (N1-2)Advanced: invades scrotal wall (T4), RP LNs (N3), visceral metastases (M1)
Testicular calcifications
Microlithiasis:0.6% males, in 50% with germ cell tumours1-2 mm calcifications in seminiferous tubulesAssociations with cryptorchidism, Kleinfelter’s, Down SyndromeLarge calcifications:Tumours - teratocarcinoma, seminoma, embryonal cell, Serrtoli and Leydig cellTeratoma - large, irregular calcificationsMiscellaneous - treated cancers, old infections, haematomas, infarcts
Locations of undescended testis
Occurs in 0.3% adult males; higher risk of torsion and malignancy (x30 risk)Root of scrotum (50%)Inguinal canal (20%)Abdominal (10%) - anywhere between lower pole of kidney and internal ring10% bilateral
Testicular torsion
Extravaginal (fetus / neonatal): twisting of testis, epididymis and tunica vaginalis in spermatic cordIntravaginal (usually peripubertal): associated with bell clapper deformity (tunica surrounds testis - 12% males)10% bilateral, difficult to palpate testis; Doppler approaches 100% Sn; at > 4 hours enlarged and heterogenous on greyscale, usually nonsalvagable at > 24 hours.
Seminal vesicle agenesis
Unilateral SV agenesis usually due to insult before 7th week in utero, thus associated renal abnormalities:Ipsilateral renal agenesis (80%)Other renal abnormality (10%)Normal kidney (10%)Bilateral SV agenesis - CFTR mutation in 60%, associated with bilateral vas agenesis, usually normal kidneys
Penile cancer
Higher risk if uncircumcised (3/1), phimosis (25%), chronic balanitis, UVA treatment, HPVUsually SCC (95%), sarcoma (including Kaposi), melanoma, BCC, lymphomaRarely metastatic, usually from a urogenital sourceMR Gd+ for local staging
BPH
50-75% males >60 y/oMore common in Blacks, HTN, DMInvolves transitional zone - glandular tissue surrounding prostatic urethra, at proximal end veru montanumIVP - ‘J-hook’ distal ureters (due to elevated interureteric ridge) ± ureteric dilatation / tortuosity if long-standingHyperplastic nodules high signal on T2W, can be low or high on T1W
Gleason Grading of Prostate Cancer
Grade 1: well differentiated, Grade 5: Poorly differentiated (4 & 5 have potential for lymphatic spread)Overall score is sum of two predominant histological patterns summated to give overall score (2-4 well differentiated, 5-7 moderately differentiated, 8-10 poorly differentiated)
Prostate cancer - location
85% located in peripheral zoneTumour grading and size predict prognosisCancer elevates PSA x10 more than BPH
Prostate cancer stage
T stage1: only on histology or DRE2a: half of one side2c: both sides of prostate3a: extracapsular extension without seminal vesicle invasion3b: seminal vesicle invasion4: spread to sphincter / rectum / pelvic wallM stage1: regional nodes;1a: distant LNs1b: osseous1c: visceral disease
MRI Prostate cancer
Tumours in peripheral zone show relatively low T2W signal (but non-specific)T1W detects haemorrhageCancer shows early rapid enhancement then early washoutCriteria for extracapsular spread: neurovascular asymmetry, angulated gland contour, obliteration of retroprostatic angleSpectroscopy - cancers show low citrate and high choline (thus elevated choline/citrate ratio >2 SD above average for peripheral zone)Mucinous adenocarcinoma and small infiltrating cancers hardest to detect
Prostate cancer nodal and metastatic spread
LNs: Obturator, Internal and external iliac LN’s;80% with nodal disease develop bone metastases at 5 yearsOsseous: 85% osteoblastic, 5% lytic, 10% mixed; pelvis > lumbar > femur > thoracic;PSA > 58 suggests bone metastases; PSA
Anatomy and blood supply
4-6 cm long, limbs 3-6 mm thickCortex (90% of gland) from mesoderm, divided into zona glomerulosa (aldosterone), fasiculata (cortisol), reticularis (epiandrosterone)Medulla from neuroectoderm, secretes adrenaline and noradrenalineAdrenal arteries: superior (inferior phrenic), middle (aorta), inferior (renal)Adrenal venous drainage - right to IVC, left to left renal vein
Adrenal adneoma
2-10% at autopsy, 1% at abdominal CT; majority non-functioningIf no malignancy, lesion 60% (absolute) (40% relative (to enhanced) at 15 minute CTMR - if non-functioning, isointense T1W and iso-/hyperintense on T2W to liver, with drop off on out of phase
Adrenal myelolipoma
Rare, benign, encapsulated, always non-functioningCan haemorrhage spontaneously and become necroticDemonstrate intralesional fatUS: hyperechoicCT: heterogeneous ± calcification (20%; especially post haemorrhage)MR: high T1W if fat or haemorrhage, drop off out of phase if fat
Adrenal cysts
20% bilateral; may calcify even at > 1 year post haemorrhageCauses:Spontaneous, especially if coagulopathic;Post-traumatic (right > left), burns, sepsis (DIC - Waterhouse Freidrichsen), post adrenal venography (10% risk)Haemorrhagic metastases (melanoma)
Phaeochromocytoma
Catecholamine secreting from chromaffin cells of medulla85% adrenal, 8% paraaortic, 5% organ of Zuckerkandl, 1% urinary bladderCause headaches, palpitations, sweating, tremor, anxiety, HTN (but only 0.1% HTN caused by phaeo)Increased vanilmandelic acid on 24 hour urine (50%)Usually > 3 cm, solid, hypervascular; rarely calcified / cysticUptake on MIBG (80% Sn), octreotide, PETEnhances strongly on CT; ‘light bulb’ very high signal on T2W MRBx: may precipitate hypertensive crisisRule of tens: 10% bilateral / familial / malignant / extra-adrenal; 98% intra-abdominalIf extra-adrenal, called paragangliomas, 40% malignant, most common at organ of Zuckerkandl (aortic bifurcation)Syndromes: MEN (5%; usually bilateral and almost always intraadrenal) 2 and 3, NF, vHL, Sturge-Weber, Carney’s Triad, tuberous sclerosis
Adrenal carcinoma
Rare, can be functioning (causes Cushing’s, virilisation) or non-functioningAssociation with MEN 1Bimodal peak - paediatric and 40 y/oGenerally large (>12 cm), haemorrhage is poor prognostic indicator20-30% calcified, generally heterogeneous enhancement on CT
Adrenal Metastasis
If known malignancy, 38-57% adrenal nodules are metastatic (usually lung, breast, renal, melanoma)Frequently bilateral; generally large, heterogenous and poorly marginatedDelayed washout on CT, no drop off on chemical shift imagingPET most accurate - uptake > liver on PET (but clear cell renal, carcinoid and bronchoalveolar may be false negative)
Adrenal lymphoma
NHL most commonly, 70% bilateral
Cushing’s Syndrome
70% due to adrenal hyperplasia: 90% ACTH pituitary adenoma, 10% ectopic ACTH (lung, islet cell pancreatic, ovarian)20% adrenal adenomas (2-4 cm)10 % adrenal cortical carcinoma (but only 10% of these cause Cushing’s)Nonspecific adrenal hyperplasia - acromegaly (100%), hyperthyroidism (40%), HTN (15%)
Conn’s Syndrome
Due to aldosterone excess; F > M, usually 40 y/oHTN, hypokalaemia, polyuria, hypernatraemiaPrimary (Conn’s disease)75% due to aldosterone-secreting adenoma (small, low attenuation, eccentric);25% adrenal cortical hyperplasiaSecondary: RAS, reninoma
Causes of adrenal failure
Primary (cortical destruction = Addison’s):AutoimmuneInfection (fungal, TB; enlarges if acute and calcifies if chronic)Drug-inducedBilateral adrenal haemorrhageMetastasisSarcoidosisHaemochromatosisAmyloidosisSecondary (due to inadequate pituitary stimulation)
Adrenal infections
TB (calcification ± soft tissue mass ± necrosis)HistoplasmosisMeningococcusEchinococcus
MEN and Carney’s Triad
All autosomal dominantMEN 1: adrenal cortical nodules / functioning adenoma, PTH hyperplasia / adenoma, pancreatic islet cell tumour, pituitary adenoma, carcinoid tumour ± multiple lipomas ± thyroid nodulesMEN 2A: Phaeochromcytomas (more frequently extra-adrenal), medullary thyroid carcinoma, PTH hyperplasia / adenomaMEN 2B: Phaeochromcytomas (more frequently extra-adrenal), medullary thyroid carcinoma, soft tissue neuromas, ganglioneuromatosis of small intestine, Marfanoid habitusCarney’s triad: Gastric leimyogenic neoplasms, extra-adrenal phaeochromocytomas / paragangliomas, pulmonary chondromas
Adrenal collision tumour
Co-existing histologically different (benign and malignant) tumours in same gland
Normal endometrial thickness
US findings at time of ovulation (
Decreased echogenicity surrounding follicleIrregular follicular wall (crenation)Small echogenic core of tissue projecting into follicle (cumulusoophorus)Sudden complete collapse of follicle at ovulation, with fluid in pouch of Douglas
Indications and contraindications for HSG
Performed days 7-12 menstrual cycle, 4-10 mL 28% water soluble contrast6 Fr Foley catheterIndicationsInfertilityRecurrent miscarriagePostoperative following tubal ligationPreoperative before myomectomyC/I if pregnant, active pelvic infection, uterine surgery in last 3 daysNormal tubal length 12-14 cmDoxycycline occasionally given if dilated tubes / adhesions as risk of tubo-ovarian abscessComplications: Bleeding, infection, contrast reaction, uterine injury
Uterine and ovarian MRI
T2W Signal (indistinct postmenopause)Endometrium - highJunctional zone - lowPeripheral myometrium - intermediateEpithelium, mucus - highOvary (reproductive) - low stroma, high follicles
Congenital Mullerian Duct Anomalies
Prevalence of 2-3%; 50% have renal anomalies (ipsilateral agenesis is commonest, renal ectopiaClass I - absent Mullerian ducts (very rare): Agenesis vagina, uterus, uterine tubesClass II - agenesis / absent unilateral MD: Unicornuate uterusClass III - lack of MD fusion; abnormal external contour: Uterus didelphysClass IV - partial MD fusion; abnormal external contour: Bicornuate uterusClass V - septation (commonest overall anomaly); normal external contour; on HSG - intercornuate distance º:Fibrous septum - highest incidence of infertility as cannot implantComplete septate (extends to cervical canal)Partial septate (cavity alone)Class VI: Arcuate uterus (normal variant)Class VII: Associated with diethylstilboestrol exposure - causes uterine hypoplasia, T shaped uterus, increased risk clear cell cancer of vagina
Mayer-Rokitansky-Hauser Syndrome
MD dysgenesis with vaginal / uterine agenesisNormal karyotype and normal secondary sex characteristicsRenal anomaliesNormal ovaries, increased risk endometriosis
Causes of female infertility
Ovulatory dysfunction (30-40%)Hyperprolactinaemia (drugs, PRL producing tumours)PCOSTubular dysfunction (30-40%)AdhesionsTubular damageEndometriosisAdenomysosisLeiomyoma
Gestational trophoblastic disease
Chorionic tissue that undergoes hydropic change but continues to produce chorionic gonadotrophinsCauses enlarged uterus with multiple small (3-10 mm) anechoic areas in uterine cavityHydatidiform moleComplete (majority): Hydropic enlargment of chorionic villi, with multiple vesicles of varying size, rarely associated fetal tissue, causes hyperemesis gravidarum, enlarged uterus, heavy first trimester bleeding ± hydropic placental tissue passed PV, ovarian cysts (theca lutein) commonPartial / incomplete: Dysmorphic fetus (often triploid)Chorioadenoma destruens (
Choriocarcinoma
Often but not necessarily post pregnancy, can arise in ovary or testis, no recognisable villous structures with synctial and cytotrophoblasts interspersed between areas of haemorrhage and necrosisMyometrial invasion ± Haematogenous dissemination to lungs, liver, kidneys, brain and GITUS: Similar to hydatidiform moleTheca lutein cysts persisting at 3-4 months post uterine evacuation suggest residual disease
Pelvic Inflammatory Disease US
US: One third normal, fluid filled uterus, thick echogenic tubes, hydro- / pyosalipnx ± adnexal or Pouch of Douglas collections
Asherman Syndrome
Uterine cavity synechiae due to trauma, infection or D&C; can cause infertility
IUCD Complications
EmbeddingPerforationIncreased risk PID (x3 risk)Actinomycosis
Uterine TB
Usually involves fallopian tubesHSG: Almost always bilateral and asymmetrical, flask-shaped dilatation / sacculation of fallopian tubes (due to fimbrial obstruction) ± tubal calcification, with tubal shortening and rigidity; ultimately leads to obliteration of uterine cavity in later disease
Endometrial carcinoma
Commonest gynaecological malignancy, 85% adenocarcinoma, postmenopausal with unopposed oestrogen risk factors (i.e. nulliparity, failed ovulation, obesity, late menopause)Thickened endometrial stripe (>8 mm postmenopausal, >15 mm premenopausal), with thinning of inner myometrium suggestive of myometrial invasion (deep invasion if obliteration of hypoechoic layer)Stage 1 and 2 - confined to uterus; 3 & 4 extrauterineMetastasis - aortocaval and pelvic LNs, liver, lungs, brain
Endometriosis sites
Ovaries (75%) > Pouch of Douglas (70%) > broad / uterosacral ligaments (35%) > uterus and fallopian tubes > GIT (12-37%, usually rectosigmoid) > urinary tract > chest / soft tissuesRare (
Endometrioma
US: homogenous, hypoechoic / anechoic focal ovarian lesion ± hyperechoic foci in wall (predictive of endometrioma) ± internal echoes, ± sepatations; tend not to resolve on follow up.MR: Homogeneous high signal on T1W, shading on T2W (dependent layering or signal void), with low signal fibrous wall on T1W and T2WMR differential (high T1W): Dermoid, mucinous cystic neoplasms (SI
Adenomyosis
MR: Short axis measurement junctional zone ≥12 mm diagnostic, 8-12 mm indeterminateHyperintense T2W 2-4 mm foci in thickened junctional zone, often parallel to endometrial stripe
Uterine fibroids
May grow during pregnancy as oestrogen dependent, regress after menopause (if enlarging, consider leimyosarcoma)Types: Subserosal, submucosal (least common but most symptomatic), intramural (commonest)Coarse dystrophic calcification (25%) is specific findingMR: low signal T2W with well-circumscribed hyperintense rim; may have ‘bridging vessel sign’ if subserosal and exophytic (due to flow voids of uterine artery branches between mass and uterus)
Cervical carcinoma staging
I - not always visible on MRII - extends beyond uterus but to pelvic wall or lower 1/3 of vaginaIIA - vaginal extension, no parametrial invasionIIB - parametrial invasionIII - extension to lower 1/3 of vagina (IIIA), or pelvic sidewall with hydronephrosis (IIIB)IV - beyond true pelvis to bladder / rectal mucosa (IVA) or distant metastases (IVB)Stage IIA versus IIB on CTIrregular / poorly defined margins of lateral cervixProminent soft tissue strandingObliteration of periuterine fat plane
Adenoma Malignum
Form of cervical cancer, watery discharge, cluster of enhancing Nabothian cystsAssociated with Peutz Jeghers and Mucinous ovarian carcinoma
Gartner’s Duct Cyst
Inclusion cyst of Gartner’s duct (mesonephric tubules) lateral to vagina
Salpangitis Isthmica Nodosa
Diverticula like invaginations of epithelial lining herniating into myosalpinx; often associated with prior PIDRisk x10 of ectopic pregnancy
Causes of infertility
Female (70%)Ovulatory dysfunction (25%)Tubal problems (25%)Endometriosis (40%)Inadequate cervical mucus (5%)Luteal defects (poor progesterone response) (5%)Male (30%)
US Assessment of ovulation
Early: Multiple cysts grow to 10 mmDominant follicle (>14 mm) by day 8-12, 5-10% >2 dominant folliclesImpending ovulation: Thickened follicular lining with thin hypechoic layer surrounding follicle, ±crenationPost-ovulation: Disappearance of follicle, free fluid in pelvis
Ovarian hyperstimulation
Enlarged ovaries with multiple cysts, begins 3-8 days post beta hCG administration may last 6-8 weeksAscites, effusions, DIC, DVT, ectopic pregnancy
Ovarian volumes and ligaments
Volumes - 3 mL pre-menarche, 10 mL menstruating, 6 mL postmenopausalAbnormal if >18 mL premenopausal or >8 mL postmenopausalLigamentsMesovarium - ovary to posterior surface broad ligamentOvarian ligament - ovary to uterusSuspensory ligament - ovary to pelvic side wall
Ovarian tumours - benign and malignant features
Benign features: 10 cm = 40% malignant
Functional ovarian cysts
Follicular cyst (>25 mm, produce oestrogen, ±internal echoes; repeat US at 2 or 6 weeks)Corpus luteum cyst (can be 5-10 cm, produce progesterone, bleeding into / failed resorption of corpus luteum, maximum size at 8-10 weeks in pregnancy, resolve at 16 weeks)Theca lutein cysts (GTD, usually bilateral and multilocular, may measure up to 20 cm)
Paraovarian cysts
Embryonic remnant in broad ligament; 10% of adnexal masses; must see ovary separately for diagnosis
Peritoneal inclusion cysts
Nonneoplastic reactive mesothelial proliferations; extraovarian location with ‘spiderweb’ pattern of entrapped ovary only in premenopausal with hx PID / surgery; can also simulate hydrosalpinx and paraovarian cysts
PCOS
Stein-Leventhal triad: Oligomenorrhoea, hirsutism, obesityHormones: Elevated LH and LH/FSH ratio, elevated androgensBilateral enlarged ovaries (similar size bilaterally) with >5 peripherally located cysts, each >5 mm, with a hyperechoic stromaHypoechoic ovary without individual cysts (25%), Normal ovary (25%)
Benign ovarian tumour
Benign serous cystadenomaThin walled, uni- or multilocular, homogenous on CT and MR, no endo- or exocystic vegetationsBenign mucinous cystadenomaUsually larger, almost always multilocular (varying density locules), smooth walls and septae
Ovarian Ca and CA125
25% gynaecological malignancy, 65% metastatic at diagnosis; CA125 positive (>35) in 35% (early) - 80% (metastatic), but if mucinous
Epithelial ovarian tumours
Malignant serous or mucinous cystadenocarcinoma (25%)Serous 50% bilateral; Mucinous 25% bilateralEndometroid carcinoma (10-15%)30-50% bilateral; 15-30% association with endometrial cancer / hyperplasiaClear cell carcinoma (5%)Nearly all have previous endometriosis, often presents as large endometrioma with solid componentsBrenner tumour (= transitional cell tumour)Small, rarely malignant, 30% association with other ovarian tumours;Multilocular cystic mass or small mostly solid mass ± enhancement of solid componentsMR: low signal, CT: extensive amorphous calcification
Germ cell tumours
Mature teratoma (commonest and only benign germ cell tumour)Commonest benign ovarian tumour if
Sex-cord stromal tumours
Granulosa cellCommonest oestrogen producing and sex-cord stromal tumour; usually peri-/postmenopausal; associated with endometrial polyps, hyperplasia and carcinoma (3-25%), 95% bilateralFibrothecomaArise from stroma, postmenopausalHomogenous hypoechoic mass, posterior acoustic shadowing, delayed homogenous enhancement on CT with dense calcifications, Low signal on T1W and very low on T2W with scattered high signal (oedema / cystic degeneration)Commonest sex cord tumour (fibroma, 4%; thecoma 1%), Lipid rich with oestrogenic activity; association with ascites and Meigs syndrome (unilateral pleural effusion)Sclerosing stromal cell tumourBenign, usually young women; large mass with solid and cystic componentsEarly peripheral enhancement with centripetal progression on dynamic studiesSertoli and Leydig cell tumours (
Metastatic ovarian tumours
10% of all ovarian tumours, occur during reproductive yearsCommonest: Colorectal, stomachOthers: Breast, lung, contralateral ovaryKruckenberg tumour: Mucin secreting signet ring cells, usually from GIT; shows bilateral complex masses with hypointense T1W solid components and int
Ovarian tumours
- Epithelial tumours (65%)2. Germ cell tumours (15-20%) - elevated AFP and hCG if malignant3. Sex-cord stromal tumours (8%)4. Metastatic10% of all ovarian tumours, occur during reproductive years
Staging ovarian cancer
I: Limited to ovaryII: Both ovaries ± ascitesIII: Intraperitoneal metastasesIV: Extraperitoneal metastases
Ovarian vein thrombosis
Rare cause of PE, right > leftUsually due to infection, hypercoaguable state, postpartum (especially if post Caesarian Section)
Breast Anatomy
Develops from upper third of mammary ridge between upper and lower limb budsClavicle to 8th rib, sternum to mid-clavicular line; Contains 20 lobes, each made up of lobules (each 500 microns, smallest structural unit of breast)
Arterial supply of breast
(venous drainage follows same pattern)UOQ - lateral thoracic artery (br of axillary),medial / central - internal mammary (subclavian), lateral - intercostal arteriesLymph - mainly to axillary (75%), internal mammary (25%) and upper abdomen
Implant rupture
1-2% of implants ruptureExtracapsular (implant shell and fibrous capsule) - snowstormIntracapsular (implant shell only) - stepladder pattern, may also diplay ‘linguini sign’Inverted tear drop - gel bleed between inner and outer capsule
Mammography views
MLO (40-60 degrees) - should have pectoralis to level of or below nipple axis, should appear convexCC - usually allows better compression, pectoralis visible on 35%, pec-nipple distance on CC should be ≤ 1cm of MLO distanceXCCL - exaggerated craniocaudal - views axillary tail of SpenceTrue lateral - ML and LM for lesion localisationCleavage valley - between breastsSpot compression and magnifcation - further evaluation of lesion margins, regions of tissue distortionTangential - for skin lesionsRolled - if lateral roll, superior lesion moves laterally, if medial roll, superior lesion moves medially
Lesion movement from MLO to lateral
Medial lesions move up, lateral lesions move down
Mammogram tube
Mo anode with 17.9 and 19.5 keV peaks, Mo filter excludes >20 keVTube windows - Be (less filtration)Compression - reduces blur, dose, motion, exposure time, scatter; improves resolution and separates overlapping structures
Signs of malignancy on Mammogram
MarginsSpiculation (also seen in scar tissue - resolves in
BIRADs Categories
0 = inconclusive1 = negative2 = benign3 = probably benign (95% certainty; needs biopsy / excision6 = biopsy proven malignancy
Malignant features of calcifications
Size 5 calcs/cm3Clustered (not scattered)Wild, fine linear branching (dot-dash)
Breast calcifications
Popcorn - involuting fibroadenoma, rarely a papillomaFine curvilinear - walls of round mass, usually benign cystDense lucent centred - fat necrosisLinear / parallel - vascularCalcified rods - secretory diseasePleomorphic -
Breast MRI
Days 7-14 best (less physiological enhancement)Round / oval lesions with non-enhancing septations almost always fibroadenomaHeterogeneous and peripheral enhancement most common in malignant lesionsCancer usually low signal on T2W
Breast cysts
Usually dilatation of lobular acini, less often distended ducts; 3 mm macrocystRarely (
Fibrocystic breast disease
Can indicate increased risk of malignancyAtypical hyperplasia x5 riskHyperplasia, sclerosing adenoma (x2)No increased risk with cysts, FA, Fibrosis, Adenosis, duct ectasia, Mastitis, metaplasia
Fibroadenoma
Commonest benign breast lesion, usually
Phyllodes tumour (cystosarcoma phyllodes)
Rare, 30-50 y/o, rapidly enlarging, mobile, usually benign stromal tumour with 25% recurrence if incomplete excision10-15% malignant with lung metastasesMalignant tumours likely if > 3 cm, contain sarcomatous elements (10% of phyllodes show haematogenous metastasis)No spiculation and no microcalcificationUS: large, well circumscribed, low amplitude internal echoes, can have posterior enhancement or attenuationMR: rapid enhancement, indistinguishable from fibroadenoma
Pseudoangiomatous Stromal Hyperplasia (PASH)
Benign proliferative lesion of mammary stroma, particularly myofibroblastsHypoechoicMay grow / recur following excision
Gynaecomastia
True: increase in number ±dilatation of ducts, can be unilateral or bilateralPseudogynaecomastia: purely fat depositionCausesHormones, liver failure (inadequate oestrogen degradation)Drugs: reserpine, digoxin, spironolactone, cimetidine, thiazides, marijuanaTesticular tumours: seminoma, choriocarcinoma, embryonal cell carcinomaKleinfelters (increased risk breast cancer)Lung cancer
Hamartoma of breast
AKA fibroadenolipoma, proliferation of fibrous and adenomatous nodular elements, surrounded by capsule of connective tissue3-5 cm, 75% palpableMammo: sharply marginated, may appear similar to lipoma, ±visible capsuleUS: sharply defined, displaces surrounding structures, heterogeneous echo pattern
Radial scar
Idiopathic scar-like lesion, requires biopsyMammo: Architectural distortion with spiculation ±microcalcifications, usually no mass, indistinguishable from cancerUS: Irregular, poorly defined, hypoechoicMR: may appear similar to cancer
Ductal carcinoma
From ductal epithelium, 90% breast cancerDCIS if confined to duct, 30-50% proceed to invasive ductal carcinoma (breaches basement membrane of duct)Mammo: Fine linear branching calcificationsMR: not always visible, usually pronounced segmental enhancement
Invasive ductal carcinoma on imaging
Mammo: irregular mass, spiculated margin, calcification, architectural distortion, skin/nipple retraction, may be undetectable if surrounding breast same density as tumourUS: Irregular, hypoechoic, retrotumoural shadowing, vertically orientated relative to skinMR: Irregular enhancing mass with rapid enhancement then plateau / rapid washout ± peripheral enhancementWell differentiated form is Tubular cancer, slow growing spiculated lesion, rarely spreads to axillary LNs
Paget’s disease of breast
Ductal carcinoma involving nipple, usually no evident tumour mass, good prognosis, US usually not indicatedMammo: may be normal, occasionally microcalcification in subareolar region directed towards nipple
Papillary carcinoma
Ductal epithelium proliferates into villous projections, fills lumen, slow growingMammo: Well circumscribed mass, lucent halo, can occur within a cystUS: Complex solid or cystic mass, may shows as fronds projecting into a cyst
Colloid / Mucinous carcinoma
Form of ductal carcinoma with mucinous differentiationMammo: Similar to other cancers but often lower density and well circumscribed, ±lobulationUS: HypoechoicMR: high signal T2W, lobulated with slow contrast enhancement
Medullary carcinoma
Incidence peaks in 20’s, large, soft, movable tumourMammo: Well-circumscribed, smooth, ill-defined marginUS: Hypoechoic ±heterogeneous internal echoes, often posterior acoustic enhancementMR: round, well-defined borders, diffuse enhancement
Inflammatory carcinoma
Warm, erythematous, peau d’orange, painless, peaks at 30 y/oMammo: Skin thickening, usually no mass or calcifications, increased density on affected side due to trabecular thickeningUS/MR no distinctive features
Lobular carcinoma
Cells similar to those lining lobules, LCIS if confined to lobule, LCIS increases risk of invasive loblular carcinoma in both breastsLCIS usually younger women with dense breasts, has lower risk of becoming invasive than DCISUsually no specific finding on mammo or US but adjacent benign tissue often has calcification
Invasive lobular carcinoma
Usually large, often bilateral, insidious onset, less desmoplastic responese than ductal cancerMammo: early detection hard, usually asymmetric breast density / area of increasing densityUS: Hypoechoic with variable posterior acoustic shadowingMR: Similar enhancement to invasive ductal carcinoma
Mastitis
Acute = puerperal, usually staphylococcusNonpuerperal - older patients, can form abscessPlasma cell mastitis - rare aseptic subareolar inflammation, usually bilateral and symmetricalGranulomatous (rare) - TB, sarcoid
Commonly missed lesions on mammography
Invasive lobular carcinoma - only architectural distortion and asymmetric density visibleInvasive ductal carcinoma - commonest well-circumscribed lesionDCIS coexisting with atypical ductal hyperplasia on bxPalpable mass - may require spot film
Postradiation breast
Usually 50 Gy total, with 60-75 Gy boosting at lumpectomy siteDiffusely dense breast most pronounced at 6 months, almost gone after 24 monthsThickening of skin and trabecula, usually resolves in months, may progress to fibrosisCalcifications Residual tumour (although should be surgically removed originally)Benign dystrophic calcification (arise at 2 to 4 years, usually benign with central lucency)
