GI Flashcards

1
Q

Helpful videos

A

GORD
https://www.youtube.com/watch?v=-MduikwcAmE

CROHNS
https://www.youtube.com/watch?v=ZBlrm9qabVM

ITUSSUSCEPTION
https://www.youtube.com/watch?v=5KvJ3iJnCQk

COLORECTAL POLYPS
https://www.youtube.com/watch?v=Rxu7wXOxlBY

GALLSTONES
https://www.youtube.com/watch?v=UPw3ot1M_o0

APPENDICITIS
https://www.youtube.com/watch?v=r9amif1DQMc

UC
https://www.youtube.com/watch?v=QPolcKbTgIE

PEPTIC ULCER DISEASE
https://www.youtube.com/watch?v=E0IBMWQDEH4

DIABETES https://www.youtube.com/watch?v=5p3pds_YtoY

PANC NETS https://www.youtube.com/watch?v=iJcFPWLdKLc

AUTOIMMUNE HEPATITIS
https://www.youtube.com/watch?v=aC0_yOlfY4U

WILSONS DISEASE
https://www.youtube.com/watch?v=Cr8R_bnKAtk

PORTAL HYPERTENSION
https://www.youtube.com/watch?v=VTnAp-ngAXw

CHRONIC CHOLECYSTITIS
https://www.youtube.com/watch?v=aU1lWPzUZgY

ALCOHOLIC LIVER DISEASE
https://www.youtube.com/watch?v=RudR2_VVoaw

CHRONIC PANCREATITIS
https://www.youtube.com/watch?v=met9SntRZe8

JAUNDICE
https://www.youtube.com/watch?v=gIACp5js4MU

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2
Q

Esophagus anatomy

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A ring is muscular ring above vestibule

B ring is mucosal ring below vestibule. Thin constriction at GOJ. SYmptomatic dysphagia can occur if it narrows. If its narrowd and symptomatic its called Schatzki ring.

Z line is squamocolumnar junction. Endoscopic finding.

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3
Q

Diverticulae in neck

A

ZENCKERS
Posterior in hypopharynx

KILLIAN JAMIESON
Anterolateral in upper esophagus

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4
Q

Reflux esophagitis

A

Common cause of fold thickening.
Mild fold thickening - severe - Strictures/Barretts - fundoplication after failed medical therapy - cancer - esophagectomy

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5
Q

Barrets esophagus

A

Precursor to adenocarcinoma, develops secondary to chronic reflux. High stricture with associated hiatal hernia. Reticular mucosal pattern.

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6
Q

Feline esophagus

A

Aunt Minnie. Transient fine transverse folds which course mid and lower esophagus. Can be normal but high association with reflux esophagitis.

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7
Q

Cancer

A

On fluoro want to see irregular contour and shouldered/abrupt edges.

SQUAMOUS
Drinking/smoking/alkaloid ingestion. Stricture/ulcer/mass mid esophagus

ADENOCARCINOMA
Chronic reflux. Barretts. Stricture/ulcer/mass in lower esophagus

CRITICAL STAGE
T3 (adventitia) vs T4 (invasion into adjacent structures). Early stages distinguishable via endoscopy but T3 and T4 need CT.

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8
Q

Hiatal hernia

A

TYPE 1 SLIDING
Most common 95%. Small ones asymptomatic but do have association with reflux if function of GEJ is impaired.
GEJ above diaphragm

TYPE 2 ROLLING PARAESOPHAGEAL
Higher rate of incarceration
GEJ below diaphragm

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9
Q

Fundoplication

A

Gastric fundus wrapped around lower end of esophagus and stitched in place reinforcing lower esophageal sphincter. Nissen is 360 degree wrap. Indications are hiatal hernia or reflux.

EARLY COMPLICATION
Esophageal obstruction/narrowing. Post op oedema or wrap too tight. Week 2.

FAILURE
Recurrence of either hernia or reflux. Usually telescoping of GEJ through wrap ‘slipped Nissen’

SLIPPED NISSEN
Usually short esophagus (‘hiatal hernia that is fixed/non-recueible, and >5cm’)

Fundoplication wrap should have length of narrowed esophagus <2cm. Anything more suggests slipped wrap.

SHORT ESOPHAGUS
Definition as above. Treatment is collis gastroplasty (lengthening and fundoplication)

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10
Q

Candidiasis

A

HIV or transplant patient (immunocompromised). Achalasia or scleroderma as motility disorders also at increased risk.

Discrete plaque like lesions. Nodularity, granularity and fold thickening as result of mucosal inflammation/oedema.

Shaggy irregular luminal surface.

GLYCOGEN ACANTHOSIS
Mimic of candidiasis. Epithelial collection of glycogen. Multiple elevated benign nodules in asymptomatic elderly patient.

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11
Q

Esophageal ulcers

A

HERPES
Small and multiple with halo of oedema

CMV and HIV
Large, flat, ovoid ulcer

CROHNS
Esohpageal involvement is rare. get aphthous ulcers which are discrete ulcers surrounded by mounds of oedema

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12
Q

Esophageal duplication cysts

A

Seen on CT mainly.

Posterior mediastinum with ROI showing water density. Most common location is in ileum with esophagus being 2nd. Usually seen incidentally in an adult or if big enough can present in an infant with dysphagia/breathing problems. Bening.

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13
Q

Esophageal diverticulum

A

ZENKER DIVERTICULUM
Pulsion diverticulum posteriorly. Always occur at Killian dehiscence/triangle. Arise from hypopharynx.

KILLIAN JAMIESON PULSION DIVERTICULUM
Anterior and lateral. Area of weakness below attachment of cricopharyngeus and lateral to muscles that helo suspend the esophagus on the cricoid cartilage. Cervical esophagus.

TRACTION DIVERTICULUM
Mid esophageal and often triangular. Occur from scarring (granulomatous disease or TB)

EPIPHRENIC DIVERTICULA
Just above diaphragm, usually on right. Pulsion type.

ESOPHAGEAL PSEUDODIVERTICULOSIS
Dilated submucosal glands causing multiple small outpouchings. Chronic reflux. Association with esophageal strictures and candidiasis.

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14
Q

Papilloma

A

Most common benign mucosal lesion of esophagus. Hyperplastic squamous epithelium

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15
Q

Eosinophilic esophagitis

A

Young man with long history dysphagia. Barium shows concentric rings. Fail PPIs but get better with steroids.

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16
Q

Esophageal web

A

Cervical esophagus near crico. See ant and post (is a ring). caused by a thin mucosal membrane. RF for esophageal and hypopharyngeal carcinoma.

Plummer Vinson syndrome: iron def anaemia, dysphagia, thyroid issues and spoon shaped nails.

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17
Q

Esophageal spasm

A

Corkscrew tertiary contractions favouring distal esophagus. Nutcracker requires manometry >180mmHg

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18
Q

Dysphagia Lusoria

A

Syndrome refers to problems swallowing secondary to compression from aberrant right subclavian artery.

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19
Q

Dilated esophagus

A

ACHALASIA
Motor disorder where distal 2/3 esophagus (smooth muscle part) has absent primary peristalsis. Lower esophageal sphincter wont relax. Birds beak at GOJ. Vigorous achalasia is early/less severe form which has repetitive simultaneous non-propulsive contractions. More common in women. Increased risk of Candida. Chagas disease is achalasia from parasite transmitted by a fly.

PSEUDOACHALASIA
Appearance of achalasia but secondary to cancer at GOJ. Real achalasia will eventually relax.

SCLERODERMA
Involves esophagus 80% time. Lower 2/3 stops working normally. LES is incompetent and end up with chronic reflux causing scarring, Barretts and pssible adenocarcinoma. Lung changes usually NSIP (groun glass sub pleural sparing). Hide bound valvulae in small bowel.

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20
Q

Varices

A

Linear serpentine filling defects causing scalloped contour.. Differential is varicoid carcinoma. Want them to flatten out on distended esophagus.

UPHILL
Portal HTN
Confined to bottom half esophagus

DOWNHILL
SVC obstruction (catheter or tumour related)
Confined to top half esophagus

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21
Q

Stomach ulcers

A
MALIGNANT
Wider than deep
Located within lumen
Nodular, irregular edges
Folds adjacent to ulcer
Carmen meniscus sign
Can be anywhere
BENIGN
Deeper than wide
Project beyond expected lumen
Sharp contour
Folds radiate to ulcer
Hamptons line
Mostly on lesser curvature
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22
Q

Gastric tumours - GIST

A

GIST
Benign or malignant. Most common mesenchymal tumour of GIT. 70% in stomach, duodenum is second most common. Rare <40yo. Lymphadenopathy rare. Malignant ones appear aggressive with ulceration and possible perforation. If they do met, usually to liver. Association with NF1. Smoothly marginated and exophytic.

CARNEYS TRIAD
Chondroma
Extra adrenal pheochromocytoma
GIST

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23
Q

Gastric tumours - adenocarcinoma

A

Most common gastric malignancy 90%. Usually disease of older person around 70. H.Pylori is RF. Can obstruct if it involves antrum. Metastatic spread to ovary is terms Krukenberg tumour. Swollen L SCN is Virchows node.

Usually large ulcerated heterogenous mass with asymmetric wall thickening, focal and nodular.

Gastric cancer more likely than lymphoma to: cause outlet obstruction, be in distal stomach, extend beyond serosa and be a a focal mass

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24
Q

Gastric tumours - lymphoma

A

Can be primary MALT or secondary systemic lymphoma. Stomach most common extranodal site for NHL.

Rarely causes gastric outlet obstruction even when extensive. Can cross pylorus. Multiple looks (big, small, ulcerative, polypoid or target lesion. Can rupture without treatment.

Classic is diffuse wall thickening without gastric outlet obstruction

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25
Mets to stomach
Rare, Melanoma is most common sulprit. Variable appearance with multiple button type soft tissue nodules. Breast and lung are other possibilities and these are known for having particular look of diffuse infiltration and a contracted desmoplastic deformity resembling a stiff leather bottle. 'linitis plastica' although this can be lymphoma too.
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Misc gastric conditions
CHRONIC ASPIRIN THERAPY Multiple gastric ulcers. 80% of chronic aspirin users get them. No duodenal ulcers. Multiple duodenal ulcers think Zollinger Ellison AREAE GASTRICAE Normal fine reticular pattern seen on double contrast. Enlarges in elderly and people with H.Pylori. Obliterated by cancer or atrophic gastritis MENETRIERS DISEASE Idiopathic gastropathy with rugal thickening tha classically invovles fundus and spares the antrum. Low albumin. Bimodal. RAMS HORN DEFORMITY Tapering of antrum. Can be seen with scarring via peptic ulcers, granulomatous disease (Crohns, Srcoid, TB and Syphilis) or schirrous carcinoma. Stomach most common GIT location for sarcoid GASTRIC VOLVULUS Organoaxial - greater curvature flips over lesser. More common Mesenteroaxial - twisting over mesentery. Can cause ischaemia and needs to be fixed. More common in kids. GASTRIC DIVERTICULUM Most commonly in posterior fundus. Dont call it adrenal mass GASTRIC VARICES Splenic vein thrombus can cause isolated gastric varices
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Gastric band surgery
Inflatable silicone band around upper part of stomach creates a restrictive pouch. Goal is to make patient feel full and not want to eat. Stomal stenosis is most common comp (too tight) with vomiting as presentation. Rarely, gastric band erosion and gastric leak can occur from pressure related ischaemia. Band slippage. Band should be positioned around 2oclock and have phi angle 4-58 degrees. If angle is off, may have slipped
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Roux en Y
Stomach divided to make a pouch. Gastric pouch attached to end-end to divided jejunum. Excluded stomach goes to duodenum as normal. The proximal jejunum is attached end-side (Y) to the other part of the jejunum. Can be done for weight loss or cancer. Less reflux and less risk of recurrent gastric cancer. Increased risk for leaks, gallstones, fistulas and internal hernias.
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Bilroth procedures
BILROTH 1 Pylorus removed and prox stomach sewed to duodenum. Done for gastric cancer, pyloric dysfunction or ulcers. Less post op gastritis cf B2. More early post op complications cf B2. BILROTH 2 Partial gastrectomy, stomach attached to jejunum. Done for gastric cancer, ulcers. Risks of dumping syndrome, afferent loop syndrome, increased risk of gastric cancer 10-20 years post op
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Upper GI surgery complications
``` AFFERENT LOOP SYNDROME Something extrinsic (adhesions, internal hernia or neoplasm) or intrinsic (scarring, oedema) obstructs upstream/afferent limb causing secretions, bile and pancreas juice to build up. Presents with belly pain and vomiting. Fluid filled U shaped loop of bowel adjacent to pancreas. Pressure dilates gb and can cause pancreatitis. ``` DUMPING SYNDROME Group of symptoms; diarrhoea, nausea, light headed/tired after meal caused by rapid gastric emptying. Bilroth 2 and Roux en Y. Related to rapid transit of undigeste food from the stomach. Therapy is conversion of Bilroth 2 to Roux en Y. CANCER Old peptic ulcer surgeries like Bilroths, 3-6x increased risk of getting adenocarcinoma within gastric remnant 15ish years after surgery BILE REFLUX GASTRITIS Fold thickening and filling defects in stomach after Bilroth 1 or 2 likely result of bile acid reflux. JEJUNOGASTRIC INTUSSUSCEPTION Rare complication, jejunum herniates into stomach. High mortality with acute form.
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Upper GI surgery complications continued
LEAK Occur early <10 days usually at gastrojejunal anastomosis. Water soluble fluoro supine to look. Dont use barium. GASTROGASTRIC FISTULA Roux en Y patients with weight gain years after surgery. Anastomotic break down is a chronic process and not painful. MARGINAL ULCER Ulcers at or near gastrojejunal anastomosis. Most common just distal to anastomosis. Small bowel not used to being exposed to stomach acid. Solitary and variable in size. If multiple or large, think chronic jejunal ischaemia.
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Upper GI surgery complications continued SBO
SBO Adhesions, internal hernias, anterior body wall hernias and strictures. Mechanical vs ileus vs closed loop. SIMPLE Single lead point for simple mechanical obstruction. Accumulation of upstream gas causes gaseous dilatation. Distension then increased by retention of fluids from decreased absorption and exaggerated intestinal secretion. CLOSED LOOP 2 or more points of obstruction. Two components the closed loop which will distend quickly from secretion and venous stasis and the supralesional component which will distend slower than closed loop. 3 beak sign with two beaks at the twist adjacent to eachother and the third more distal. If there is a radial layout you may see vessels and loops converging to point of obstruction. Pneumatosis common. In coronal, can see C or U shaped fluid filled loops. ROUX EN Y OBSTRUCTION Obstruction of Roux limb with dilated gastric pouch and jejunal Roux limb. Decompressed sotmach and duodenum Obstruction of biliopancreatic limb is closed loop (blind ended) and high risk ischaemia/perforation. Dilated stomach and duodenum with decompressed gastric pouch and Jejunal Roux limb. Obstruction below JJ anastomosis. Everything may be dilated. Adhesions most common however weight loss can cause this as well with less protective mesenteric fat
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Upper GI surgery complications continued
INTERNAL HERNIA Antecolic or retrocolic. This describes the passage of Roux limb as either in front or behind the transverse colon. If retrocolic, need small defect in transverse mesocolon to pull Roux limb through which is source for internal hernia HERNIA SITES Defect in transverse mesocolon. Mesenteric defect at enteroenterostomy - hole in mesentery near JJ anastomosis. Behind Roux limb mesentery (Petersen) with antecolic or retrocolic.
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Fluoro bowel folds
THIN STRAIGHT WITH DILATATION Obstruction, ileus, scleroderma, sprue THICK STRAIGHT SEGMENTAL DISTRIBUTION Ischaemia, radiation, haemorrhage, adjacent inflammation THICK STRAIGHT DIFFUSE DISTRIBUTION Low protein, venous congestion, cirrhosis THICK FOLDS WITH NODULARITY SEGMENTAL Crohns, infection, lymphoma, mets THICK FOLDS WITH NODULARITY DIFFUSE Whipples, lymphoid hyperplasia, lymphoma, mets, intestinal lymphangiectasia
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Fluoro bowel loop separation
SEPARATION WITHOUT TETHERING Ascites, wall thickening, adenopathy, mesenteric tumours SEPARATION WITH TETHERING Carcinoid
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Fluoro bowel nodules
SAND LIKE Whipples, Pseudo Whipples UNIFORM 2-4mm Lymphoid hyperplasia NODULES OF LARGE OR VARYING SIZE Mets (melanoma) COBBLESTONING Crohns
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Fluoro bowel trademark features
RIBBON BOWEL Graft vs Host HIDEBOUND BOWEL Scleroderma ``` MOULAGE SIGN (TUBE OF WAX) Coeliac ``` FOLD REVERSAL Coeliac WORM LIKE Ascaris suum TARGET SIGN Single target: GIST, primary adenocarcinoma, lymphoa, ectopic pancreatic rest, met Multiple target: lymphoma, met CLOVER LEAF SIGN Healed peptic ulcer of duodenal bulb
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Small bowel path
WHIPPLES Rare infection Tropheryma Whipplei. White men in 50s. Infiltrates lamina propria with large macrophages. Swelling intestinal villi, thickened irregular mucosal folds. Buzzword sandlike nodules. PSEUDO-WHIPPLES MAI infection. Seen in AIDS with CD4<100. Differentiate with acid fast stain (MAC positive) INTESTINAL LYMPHANGIECTASIA Obstruction to flow of lymph from small intestine to mesentery. Dilation of intestinal and serosal lymphatic channels. GRAFT VS HOST Ribbon bowel. Patients after bone marrow transplant. Skin liver andGIT hit. Bowel is featureless , atrophic with fold thickening. SMA SYNDROME Compression of D3 by SMA in midline. Stomach D1 and D2 will be dilated. Seen in patients with rapid weight loss
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Small bowel path continued
COELIAC SPRUE Small bowel malabsorption of gluten. Malabsorption of iron leads to iron deficiency anaemia. Associated with idiopathic pulmonary haemosiderosis. Gold stanard is biopsy. Get fold reversal, cavitatory lymph nodes and splenic atrophy MECKELS DIVERTICULUM Congenital true diverticulum of distal ileum. Persistent piece of omphalomesenteric duct. 2% population, 2 types of heterotropic mucosa (gastric/pancreatic), 2 feet from IC valve, 2 inches long. Can get diverticulitis in it, GI bleed from gastric mucosa, lead point for intussusception, can cause obstruction. DUODENAL INFLAMMTORY DISEASE Fold thickening of duodenum from adjcent inflammation of pancreas or gallbladder. Can get fistula formaion from Crohns. Chronic dialysis patients can get severely thickened duodenal folds. JEJUNAL DIVERTICULOSIS Occurs along mesenteric border. Important association with bacterial overgrowth and malabsorption. GALLSTONE ILEUS Mechanical obstruction secondary to passage of gallstone to lumen of bowel. Usually by eroding through duodenum. Riglers triad of pneumobilia, obstruction and ectopic location of gallstone
40
Bowel trauma
DIRECT SIGNS Spilled oral contrast Active mesenteric bleed INDIRECT SIGNS Fat stranding Fluid layering along the bowel.
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Shock bowel vs bowel trauma
BOWEL TRAUMA Focal Wall thickening with hygh attenuation blood in submucosa. Mucosa enhances normally. Secondary signs of injury (free air, contrast leak) SHOCK BOWEL Diffuse Wall thickening with near water attenuation oedema. Mucosa demonstrates intense enhancement Other signs of shock (bright adrenals, flat IVC etc, hypoenhancement of solid organs, bilateral delayed nephrograms)
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Small bowel cancer
ADENOCARCINOMA Most common in prox small bowel (usually duodenum). Increased incidense with coeliac and enteritis. Focal circumferential wall thickening. More likely to obstructive than lymphoma LYMPHOMA Usually NHL. Coeliac, AIDS, SLE higher risk. Can look like anything. Usually do not obstruct. Favours ileum. CARCINOID Mass (often with calcs) with desmoplastic stranding. Commonly in young adults. Primary tumour often not seen. Liver mets often hypervascular. Dont get carcinoid syndrome (flushing/diarrhoea) until mets to liver. Most commonly mass is in distal ileum. MIBG or octreotide scan. METS Usually melanoma which hits small bowel in 50% fatal cases. Can get haematogenous seeding of small bowel with breast, lung and Kaposi Sarcoma. Multiple targets.
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Hernias
SPIGELIAN Lateral ventral. Location along semilunar line (lateral border of rectus). Usually above arcuate line. LUMBAR Superior: More common, congenital or acquired (surgery/trauma). Through triangle of 12th rib/QL/IO Inferior: less common, congenital or acquired. Through triangle Lat dorsi/EO/iliac crest LITTRE Hernia with Meckel diverticulum in AMYAND Hernia with appendix in RICHTER Contains only one wall of bowel, does not obstruct but high risk for strangulation. OBTURATOR Old lady hernia. Increased intra-abdominal pressure. Asymptomatic but can strangulate. Parasthesia along inner thigh from compression of obturator nerve (Howship Romberg sign)
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Femoral vs direct vs indirect
FEMORAL Old ladies. inferor to inferior epigastric and medial to common femoral vein. Below pubic tubercle. Can compress femoral vein. Narrow hernia neck, obstruction common DIRECT Less common than indirect. Medial and anterior to inferior epigastric artery. Defect in Hesselbachs triangle. Above pubic tubercle. Hernia compresses inguinal canal. Not covered by internal spermatic fascia INDIRECT More common than direct. Lateral and superior to inf epigastric artery. Failure of processus vaginalis to close. Above pubic tubercle. No compression of ingunial canal contents. Covered by internal spermatic fascia
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Internal hernia
Usually manifest as closed loop obstruction. Herniation of viscera through peritoneum or mesentery. Herniation through known anatomic foramen or recess, one that has been created postoperatively. Sac like cluster of dilted small bowel loops with twisted mesenteric vessels in abnormal location in patient with obstructive symptoms Paraduodenal most common. Occur through congenital defects Lanzert and Waldeyer. LEFT sided is Lanzert. Defect in descending colon mesentary. Dilated small bowel loops in left anterior pararenal space. RIGHT is Waldeyer. Defect in ascending colon mesentery. Associated with malrotation
46
Ileus
Paralyzed bowel due to abnormality in migrating myoelectric complex. Can be from abdominal inflammation, infection, chemical/pharmacological, trauma, post op etc. GENERALIZED Large and small bowel air filled but not dilated. REACTIVE/FOCAL Localized lack of bowel movement. Classic is appendicitis, pancreatitis, diverticulitis for sentinel loop location. Gasless abdomen: No bowel gas. Non specific and cann be from diarrhoea or fluid filled bowel obstruction. Clinical context important.
47
Crohns
Bimodal: young adults 15-30 and older adults 60-70. Dicontinuous involvement entire GIT. Stomach usually involves antrum (Rams Horn). SB invovled 80% time with terminal ileum almost always involved (string sign from marked narrowing). After surgery, Neo TI will be involved often. Colonic usually right sided and spares rectum/sigmoid. Complications include fistula, abscess, gallstones, fatty liver and sacroilleitis Squaring of folds from obstructive lymphoedema Skip lesions Proud loops separatet due to mesenteric infiltration/LNs Cobblestoning in bowel wall due to longitudinal and transverse ulcers separated by oedema Filiform - post inflammatory polyps Pseuodpolyps - islands of hyperplastic mucosa Pseudodiverticula - antimesenteric side String sign - marked narrowing TI from oedema/spasm/fibrosis
48
Ulcerative colitis
Bimodal: young adult 15-40 and older adult 60-70. Favours males. Involves rectum 95% time with retrograde continuous progression. TI involved 5-10% time due to backwash ileitis. Associated with colon cancer, primary sclerosing cholangitis, and arthitis. Ahaustral colon with diffuse granular appearance to mucosa (lead pipe).
49
Crohns vs UC
CROHNS Slightly less common. Skip lesions. TI string sign. Stenosed ileocaecal valve. Mesenteric fat increased (creeping fat). LNs enlarged. Makes fistulae. Gallstones. Hepatic abscess. Pancreatitis. ULCERATIVE COLITIS Slightly more common. Continuous. Begins at rectum. Ileocaecal valve open. Perirectal fat increased. LNs normal. No fistula. PSC association. Cancer increased risk.
50
Large bowel path
TOXIC MEGACOLON UC and Crohns are primary cause. C.diff can cause it also. Gaseous distension in trv colon on upright with distension of asc and desc on supine films. Lack of haustra with pseudopolyps. Dont do barium, risk of perforation. BEHCETS Ulcers of penis and mouth. Can effect GIT and look like Crohns. Primary cause of pulmonary artery aneurysms. DIVERTICULOSIS/DIVERTICULITIS Diverticulosis bleeds more than diverticulitis. Right sided less common.Fistula formation most common with diverticulitis EPIPLOIC APPENDIGITIS/OMENTAL INFARCT Epiploic appendagitis along serosal surface of colon, mostly on left. No concentric bowel wall thickening. Antimesenteric side usually. Omental infract usually on right and on mesenteric side. APPENDICITIS Obstruction via faecolith - mucinous fluid build up - venous supply compressed - necrosis - wall breaks down - bacteria into wall - inflammation causes pain umbilicus - RLQ when parietal peritoneum contacted. 6mm size still in use. APPENDIX MUCOCOELE Mucinous cystadenoma most common mucinous tumour of appendix. Can dilate and get very big. Look similar to cystadenocarcinomas an can perofrate causing pseudomyxoma peritonei. Onion sign layering within cystc mass
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Large bowel path continued
COLONIC VOLVOLUS Sigmoid: most common adult form - old lady. Chronic constipation predisposing. Coffee bean sign. Points to RUQ calssically. 50% recurrence rate. Large bowel will be dilated. Caecal: seen in younger people 20-40. People with long mesentery. Points to LUQ. Less common. Remainder of large bowel normal calibre Caecal bascule: anterior folding of caecum without twisting. DIlated caecum in ectopic position in abdomen without twist. COLONIC PSEUDO-OBSTRUCTION Ogilvie syndrome. Seen after serious medical conditions in nursing home patients. Marked diffuse dilatation of large bowel without obstruction point. DIVERSION COLITIS/POUCHITIS Bacterial overgrowth in blind loop which gets no faeces. Classic with pre-existing inflammatory bowel disease COLITIS CYSTICA Cystic dilataiton of mucous glands. Superficial: small in entire colon. Vitamin deficiencies and tropical sprue. Deep: large seen in pelvic colon and rectum. RECTAL CEVERNOUS HEMANGIOMA Rare. Associated with Klippel Trenaunay Weber. Tons of phleboliths. GOSSYPIBOMA Retained cotton product or surgical sponge, can elicit inflammatory response.
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Large bowel infections.
ENTAMOEBA HYSTOLYTICA Parasite that causes bloody diarrhoea. Can cause liver/spleen/brain abscess. Cause of toxic megacolon. Flask shaped ulcers, coned caecum on barium. Caecum and ascending colon,spares TI COLONIC TB Another cause of coned caecum. Involes TI. Fleischner sign is enlarged gaping IC valve and narrow TI (inverted umbrella). Stierlin sign acute on chronic disease slwollen lips of IC valve COLON CMV Immunosuppressed. Deep ulcerations lead to perforation C.DIFF Seen after antibiotic therapy, high WBC. Accordian sign of enhancing oeematous mucosa or contrast trapped inside mucosal folds. Thumb printing, ulceration, irregularity. Can cause toxic megacolon TYPHLITIS/NEUTROPENIC COLITIS Limited to caecum. Severe neutropenia.
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Colon cancer
ADENOCARCINOMA Common cause of cancer death. Cancers on right tend to bleed. Cancers on left tend to obstruct. Apple core is buzzword. Large bowel intussusception in adult is malignancy. Colon mets to liver. Liver mets T1 dark T2 mildly bright. SQUAMOUS CELL CARCINOMA Occasionally in anus - HPV
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Rectal cancer
98% adenocarcinoma. If squamous - HPV. Low rectal cancer has highest recurrence rate. MRI used to stage, only really need T2. T3 when breaks out of rectum into perirectal fat. HIGH RECTAL Gets low anterior resection. Maintain faecal continence. LOW RECTAL Get abdominoperitoneal resection. Get colostomy.
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Colon misc masses
LIPOMA Second most common tumour in colon ADENOMA Most common benign tumour of colon and rectum. Villous adenoma has highest risk for malignancy. MCKITTRICK WHEELOCK SYNDROME Villous adenoma causing mucous diarrhoea leading to severe fluid and electrolyte depletion. 80yo women with diarrhoea, hyponatremia, hypokalemia, hypochloremia, mass in rectum/bowel.
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Retroperitoneal structures
Proximal 1/3 of rectum D2 and D3 Pancreas except tail Colon asc and desc
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Disease spread in abdomen
Haematogenous Lymphatic Intraperitoneal seeding via natural flow of fluid usually from pelvis to upper abdomen. Particularly right paracolic gutter, lower recess of mesentery, sigmoid mesocolon, PoD. Pelvic abscesses usually in dependednt spots when supine. Direct invasion along ligaments (gastrohepatic, gastrosplenic, duodenocolic)
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Peritoneal processes
PSEUDOMYXOMA PERITONEI Gelatinous ascites from either ruptured mucocoele or intraperitoneal spread of mucinous neoplasm (ovary/colon/appendix/pancreas). Buzzword is scalloped appearance of liver PERITONEAL CARCINOMATOSIS Natural flow of ascites dictates location. Retrovesical space is most common spot. OMENTAL SEEDING/CAKING Omental surface can get implanted and become thick. Posterior displacement of bowel from ant abdo wall PRIMARY PERITONEAL MESOTHELIOMA 75% invovles lungs but 25% is involving peritoneal surface. Occurs 30-40 yers after initial exposure CYSTIC PERITONEAL MESOTHELIOMA Not associated with asbestos exposure. rare and benign. WOmen of child bearing age.
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Barium complications
PERITONITIS Attack of peritoneal barium by leukocytes causes large inflammatory reaction. Massive ascites, hypovolemia and shock. Long term granulomas and adhesions. INTRAVASATION If in systemic circulation, 50% get PE. Increased rsk in inflammatory bowel or diverticulitis
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Mesenteric masses
CYSTIC UNILOCULAR Duplication cyst, lymphocoele, pseudocyst CYSTIC MULTILOCULAR Lymphangioma SOLID MANY Mets, lymphoma, mesothelioma SOLID SINGLE Liposarcoma, GIST, solitary fibrous tumour, carcinoid, desmoid, sclerosing mesenteritis
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Mesentery
MESENTERIC LYMPHOMA Usually NHL. Sandwhich sign. Confluent soft tissue mass encasing mesenteric vessels. MISTY MESENTERY Increased mesenteric fat density around jejunal root often with a few small nodes, Usually mesenteric panicullitis but can be lymphoma.
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Couinad system
Divides liver into functional segments, each with own biliary drainage, inflow and outflow. Right hepatic vein divided segments 7/8 and 6/5 Middle hepatic vein divides 4a/8 and 4b/5 Left hepatic vein divides 4a/2 and 4b/3 Portal vein divides liver into upper and lower segments Caudate lobe drains directly to IVC Cantlies line divides liver into functional left and right lobes. IVC to middle of gb fossa.
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Caudate lobe
Direct connection to IVC through its own hepatic veins which dont communicate with primary hepatic veins. Supplied by branches of left and right portal veins. Caudate spared or hypertrophied in various pathologies.
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Right portal vein
Longer intrahepatic course - right lobe first o develop fibrosis and atrophy - right lobe most likely to have hepatic abscesses
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Portal hypertension
Increased hepatic resistance PREHEPATIC Portal vein thrombosis, tumour compression HEPATIC Cirrhosis, schistosomiasis POST HEPATIC Budd Chiari
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Transient Hepatic Attenuation Differences THAD
Arterial buffer responses. CIRRHOSIS Scar/fibrosis deforms hepatic sinusoids and compresses the small portal veins. Usually subcapsular CLOT Clot in portal vein MASS Direct mass effect on veins Upregulation of arterial flow ABSCESS/INFECTION Hyperaemia or mass effect
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Multifocal HCC
Regenerative nodules (T2 dark) - dysplastic nodules - HCC (T2 bright) Nodules change from drinking portal venous blood to arterial blood. HCC has arterial enhancement and rapid washout. Remember cirrhotic livers squeeze out benign lesions. Lesion within cirrhotic liver is suspicious
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Liver nodules
REGENERATIVE Contains iron T1 variable, T2 dark. Does not enhance DYSPLASTIC Contains fat, glycoprotein T1 bright, T2 iso/dark Usually does not enhance HCC T2 bright Does enhance
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MRI contrast
Gadolinum bound to chaltionagent. SHortens T1 time Etracellular vs hepatocyte specific
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hepatic hemangioma
Most common benign liver mass. Women 5:1. ENlarge wth pregnancy. No doppler flow Dicontinuous nodular peripheral enhancement with progressive fill in
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Focal Nodular Hyperplasia FNH
Second most common benign liver mass. May start in utero as AVM. Composed of normal hepatocytes, abnormally arranged ducts and Kupffer cells. Spoke wheel on USS Homogenous on arterial CT Stealth lesion on MRI Scar will show delayed enhancement Must hit scar with needle to get adequate biopsy. Can develop after chemo. 30-40% hot on sulfur colloid. Birth control pills may promote growth.
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Hepatic adenoma
Solitary lesion in females on OCP or man on anabolic steroids. If multiple, glycogen storage disease (Von Gierke). Most common location right lobe liver. 5cm often cutoff for resecting. May degenerate into HCC after long period of stability. Often regress after OCP stopped. Propensity to bleed. Subtypes: Inflammatory, HNF-1 alpha mutated, beta catenin mutated
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HCC
Occurs in setting of cirrhosis and chronic liver disease, Hep B, Hep C, haemachromatosis, glycogen storage disease, alpha 1 antitrypsin. AFP elevated in 80-95% Will often invade portal vein. Can cause spntaneous hepatic bleeds. Cancer of hepatocyte
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Fibrolamellar HCC
Younger patients without cirrhosis and normal AFP. Buzzword central scar which does not enhance (FNH does). Tumour is gallium avid. Calcifies more than HCC
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Cholangiocarinoma
Cancer of bile duct. Classic is 80yo man with PSC (or ulcerative colitis), recurrent pyogenic oriental cholangitis, Caroli disease, hepatitis, HIV, history of cholangitis, thorotrast. Scar generating cancer. Mass that enhances on delayed imaging or secondarily through the desmoplastic pulling of the scar (capsular retraction and ductal dilatation). Painless jaundice. HCC invades portal vein, cholangiocarcinoma encases it. Delayed enhancement, peripheral biliary dilatation, liver capsular retraction, NO tumour capsule Proximal extent of involvement is a key factor for surgical candidacy (more is bad). Atrophy of a lobe implies biliary +/- vascular involvement of that lobe. Bilateral involvement is bad news, veins on right and ducts on left.
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Klatskin tumour
Cholangiocarcinoma at bifurcation of left and right hepatic ducts. Small but causes biliary obstruction (shoulder/abrupt tapering).
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Cancer markers
Cholangio: raised CEA, raised CA 19-9 Panc Ca: Normal CEA, raised CA 19-9 Colon Ca: Raised CEA, normal CA 19-9
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Hepatic angiosarcoma
Very rare though most common primary sarcoma of the liver. Associated with toxic exposure - arsenic use, thorotrast, polyvinyl chloride, radiation. Can be in haemochromatosis and NF1
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Biliary cystadenoma
Uncommon benign cystic neoplasm of liver. Middle aged women. Pain or jaundice. Uni or multilocular. No reliable way to distinguish from biliary cystadenoma.
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Mets to liver
Much more common than primary. Think colon first. Calcified mets usually from mucinous neoplasm (colon ovary pancreas) Hyperechoic often hypervascular (renal, melanoma, carcinoid, choriocarcinoma, thyroid, islet cell). Hypoechoic often hypovascular (colon lung pancreas) Low density on CT with cotinuous enhancing rim
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Lymphoma
Hodgkins involves liver 60%. Non Hodgkins is around 50%
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Kaposi sarcoma
Seen in patients with AIDS. Diffuse periportal hypoechoic infiltration.
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USS review
CYSTS Anechoic, well defined thin wall. Single or multi <2cm. HEMANGIOMA Most common liver tumour, well defined homogenously echogenic. No doppler flow (slow flow lesion). Posterior enhancement. FNH Young woman. Seen after chemo. Isoechoic to liver and difficult to see unless bulging capsule or central scar. HEPATIC ADENOMA Anabolic hormones and oral contraceptives. Glycogen storage disease. ROund mass defined borders. Appearacnce variable due to haemorrhage, fat calcification and necrosis. HCC Lots of internal flow or peripheral flow on doppler. Cirrhotic liver. METS multiple lesions
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Incidental liver lesion
BENIGN FEATURES Sharp margins, density <20HU, characteristic benign enhancement SUSPICIOUS FEATURES Blurry margins, thick septa, nodular or heterogenous, density >20HU on PV imaging
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Cystic kidney disease AD or AR
ADPCKD have cysts in liver ARPCKD liver tends to be fibrotic
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Hereditary Haemorrhagic Telangiectasia (Osler Weber Rendu)
Autosomal dominant disorder characterised by multiple AVMs in liver and lungs. Leads to cirrhosis.
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Liver infections
Viral, abscess (pyogenic or amoebic), fungal, parasitic or granulomatous VIRAL HCC in setting of hepatitis can occur in acute form of Hep B. Chronic Hep C increases risk for HCC. Starry sky appearance on USS. Starry sky can just be in liver oedema making the fat surrounding the portal triads look brighter than normal. PYOGENIC Can mimic cysts. Single abscess is klebsiella and multiple is E.Coli. Gas suggests pyogenic. Central low density, rim enhancement and surrounding low density is classic sign for liver abscess. Amoebic abscess in left hepatic lobe need to be drained as they can rupture into pericardium ``` FITZ HUGH CURTIS Known PID (gonococcal salpingitis and/or chlamydia) with RUQ pain. Enhancement of anterior liver capsule, ascites and peritoneal septations. ```
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Fatty Liver
Can be focal or diffuse with sparing. Liver brighter than right kidney. Hepatosteatosis is fat liver. NASH (non alcoholic steatohepatitis) has deranged LFTs. On MRI there is drop out on out of phase. Caused by fatty diet, chemo, steroids, CF.
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Haemochromatosis
Iron overload Liver and spleen both T1 and T2 dark. In and out of phase are opposite to fatty liver with low signal on in phase and high signal on out of phase. PRIMARY Inherited, more GI uptake with resulting iron overload. Pancreas involved, spleen spared (primary = panc) SECONDARY Acquired, result of either chronic inflammation or multiple transfusions. Body reacts by trying to eat the iron. Pancreas spared, spleen not (secondary = spleen).
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Budd Chiari
Pregnant women or any hypercoagulable (most common idiopathic. Hepatic venous outflow obstruction, intra- and extrahepatic systemic collateral veins, large regenerative nodules in dysmorphic liver. Caudate lobe often massively enlarged. Liver on PV will show flip flop pattern, low attenuation centrally and high attenuation peripherally. Nutmeg liver with inhomogenous mottled appearance and delayed enhancement of peripheral liver. NUTMEG LIVER Budd Chiari, Hepatic veno-occlusive disease, right heart failure, constrictive pericarditis. Regenerative (hyperplastic) nodules difficult to distinguish from HCC. T1 bright, T2 dark. Presentation can be acute or chronic. Acute from thrombus into hepatic vein or IVC - rapid onset ascities. Chronic from fibrosis of intrahepatic veins, rpesumably from inflammation. CAUDATE HYPERTROPHY Budd Chiari, PSC, PBC
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Hepatic veno-occlusive disease
Form of Budd Chiari that occurs from occlusion of small hepatic venules. Result of chemotherapy.
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Passive congestion
Caused by stasis of blood within liver due to compromise of hepatic drainage. Common complication of CHF and constricctive pericarditis
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Misc liver conditions
``` PORTAL VEIN THROMBOSIS Hypercoagulable states (cancer, dehydration etc). Can lead to cavernous transformation with bunch of serpiginous vessels in porta hepatis. Takes 12 months ato happen ``` PSEUDOCIRHOSIS Treated breast ca mets to liver can cause contour changes, Multifocal liver retraction and enlargement of caudate CRYPTOGENIC CIRRHOSIS Cirrhosis of unknown cause. Probably non alcoholic fatty liver disease. LIVER TRANSPLANT Can double in size in 3 weeks - great for partial donation. Hep C most common disease requiring transplant. Right lobes most commonly implants. Contraindication is extrahepatic malignancy, advanced cardiac disease or pulmonary disease, active substance abuse. Normal liver portal vein gets 70% blood flow. In transplant, hepatic artery is primary source of blood flow
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Biliary
PORTAL VENOUS GAS VS PNEUMOBILIA Pneumobilia is central. Portalvenous gas is peripheral JAUNDICE Common duct stone is thought of but most common is from benign stricture (surgery or biliary intervention) BACTERIAL CHOLANGITIS Hepatic abscess can develop secondary to cholangitis, usually as result of stasis. PRIMARY SCLEROSING CHOLANGITIS Chronic cholestatic liver disease of unknown etiology characterized by progressive inflammation which leads to multifocal strictures of the intra and extrahepatic bile ducts. Often results in cirrhosis. Strongly associated with cholangiocarcinoma. Buzzword for cirrhotic pattern is central regenrative hypertrophy. Associated with UC. Indication for transplant. Withered tree or beaded appearance AIDS CHOLANGIOPATHY Infection of biliary epithelium, classicaly cryptosporidium. Can cause ductal disease in AIDS. Mimics PSC. Papillary stenosis.
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AIDS cholangiopathy vs PSC
AIDS CHOLANGIOPATHY Focal strictures of extrahepatic duct >2cm Absent saccular deformities of ducts Associated papillary stenosis PSC Extrahepatic strictures rarely >5mm Has saccular deformities of ducts
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Oriental cholangitis
Recurrent pyogenic cholangitis. South East Asia. DIlated ducts full ofpigmented stons. "straight rigid ducts". Cause not known, major risk factor for chlangiocarcinoma
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Primary biliary cirrhosis PBC
Autoimmune disease resulting in destruction of small and medium ducts. Affects middle aged women. Irregular dilatation of intrahepatic ducts with normal extrahepatic ducts. Increased risk HCC. Antimitochondral antibodies 95% time
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Long common channel
Anatomic variant where CBD and panc duct fuse prematurely in panc head. Increased risk pancreatitis. Also association with type 1 choledocaocysts
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Choledochal cysts/Carolis
COngenital dilatations of bile ducts TYPE 1 Focal dilatation of CBD, fusiform and extrapancreatic. TYPE 2 Saccular. Essentially diverticulum of CBD TYPE 3 Choledococoele. Fusiform dilatation in panc head TYPE 4 Separate dilataions intra hepatic and extrahepatic. TYPE 5 Carolis disease. Intrahepatic only
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Carolis
Autosomal recessive associated with PCKD and medullay sponge kidney. Intrahepatic duct dilatation that is large and saccular. Central dot sign is portal vein surrounded by dilated bile ducts Complications Cholangiocarcinoma, cirrhosis, cholangitis, intraductal stones. Can get stones in them and get recurrent infecion
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Ductal summary
CAROLIS Communicates with ducts. Type 5 cyst. Central dot sign. Associated with PCKD, medullary sponge and cholangiocarcinoma PSC 40yo male with UC. Withering tree. Beading. Mild dilatation. Strongly associated with ulcerative colitis and cholangiocarcinoma. ``` ORIENTAL CHOLANGIOHEPATITIS (RECURRENT PYOGENIC) Associated with clonorchiasis, ascariasis. Lots of stones. Favors left ductal system. Strongly associated with cholangiocarcinoma. ``` AIDS CHOLANGIPATHY Related to cryptosporidium or CMV. Segemental strictures, looks like PSC. Ducts look like PSC, papillary stenosis. Associated with cholangiocarcinoma. Ca stricture long andshouldered Benign strictures abrupt and short
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Gallbladder variants
PHYRIGIAN CAP GB folds on itself. means nothing. INTRAHEPATIC GB Variants in location are rare. This one found above interlobar fissure. DUPLICATED Can happen DUCT OF LUSCHKA Accessory cystic duct. Can be a cause of persistent bile leak after cholecystectomy
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GB path
WALL THICKENING >3mm. Non specific from biliary (cholecystitis, AIDS, PSC) or non biliary (hepatitis, heart failure, cirrhosis). GALLSTONES 10% asymptomatic patients. 75% cholesterol, 25% pigmented. GB SHADOWING Full of stones. Porcelain GB. Emphysematous cholecystitis MIRIZZI SYNDROME Common hepatic duct obstructed secondary to impacted cystic duct stone. Stone can eventually erode into CHD or GIT. GB cancer 5x risk with Mirizzi. Occurs more with low cystic duct insertion allowing for more parallel course and closer proximity to CHD
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Adenomyomatosis vs cholesterolosis
ADENOMYOMATOSIS Hypertrophied mucosa and muscularis propria with choelsterol crystals deposited in an intraluminal location (within Aschoff Rokitansky sinuses) CHOLESTEROLOSIS Cholesterol and triglyceride deposition within substance of lamina propria. Associated with cholesterol polyps
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GB path continued
PORCELAIN GB Extensive wall calcification. Increased risk of GB cancer. Removed. ``` POLYPS Cholesterol (most common, enlarged papillary fronds full of lipid filled macrophages attached by stalk) or non cholesterol (adenomas, papillomas). Non cholesterol usually solitary and large. Not mobile, dont shadow. Pedunculated, small and multiple with comet tail is benign. Large, sessile, solitary with flow is malignant. ``` GB CANCER Elderly woman non specific RUQ pain, weight loss, anorexia, history of stones, PSC or large polyps. 85% associated with stones. Mirrizi increases risk. Porcelain GB increase risk. Often present late wth tumour invasion into liver or portal nodes.
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Doppler
``` Duplex = colour Spectral = colour with waveform ``` Thing needing blood all the time have continuous diastolic flow and low resistance. Angle <60
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Tardus parvus
TARDUS Slowed systolic upstroke. Accelration time ?0.07 sec is >50% stenosis. PARVUS Decreased systolic velocity. Measure by change in velocity from end diastole to first systolic peak. Acceleration index <3m/s is >50% stenosis.
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Stenosis
DIRECT SIGN Found at stenosis itself. Elevated PSV and spectral broadening (immediate post stenotic) INDIRECT SIGN Tardus parvus downstream. RI downstream low <0.5, RI upstream high >0.7.
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Hepatic vein
Flow should be antegrade, liver to heart. Things that alter waveform are going to be pressure changes in heart transmitted to hepatic veins (CHF, tricuspic regurg) or compression of veins directly (cirrhosis) INCREASED HV PULSATILITY Tricuspid regurg Right sided CHF DECREASED HV PULSATILITY Cirrhosis Hepatic venous outflow obstruction
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Portal vein
Flow should always be toward liver. 20-40m/s. Waveform gentle undulation. PV PULSATILE Right sided CHF, tricuspic regurg, cirrhosis PV REVERSED Portal HTN ABSENT FLOW Thrombosis, tumour invasion, bad portal HTN SLOW FLOW Portal HTN. Pre (portal vein thrombosis), intra (cirrhosis), post (right heart failure, tricuspid regurg, Budd CHiari)
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Pancreas imaging trivia
Brighter than liver on USS. Brightest organ on T1 MRI
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Cystic fibrosis in pancreas
85-90% CF patients have panc involved. Insipissated secretions cause prox duct obstruction leading to - fibrosis - fatty replacement Panc CF diagnosed as adults have more problems than those diagnosed as kids. Residual panc function get bouts of pancreatitis Complete fatty replacement most common imaging findings in adult Markedly enlarged with fatty replacement is lipomatous pseudohypertrophy Fibrosing colonopathy is wall thickening of prox colon as complication of enzyme replacement
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Shwachman Diamond syndrome
2nd most common cause of panc insufficiency in kids (CF first). Kid with diarrhoea, short stature (metaphyseal chondroplasia) and eczema.Also causes lipomatous pseudohypertrophy of pancreas.
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Pancreatic lipomatosis
Most common pathologic condition involving pancreas. Most common chidhood cause CF. Others are cushings, steroids, hyperlipidemia, Swachman Diamond. Lipomatosis vs Agenesis. Agenesis will not have a duct.
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Dorsal pancreatic agenesis
Sets you up for diabetes (beta cells in tail), associated with polysplenia.
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Annular pancreas
Failure of ventral bud to rotate with duodenum. Encasement of duodenum. Rare cause of duodenal obstruction. DUodenal obstruction in kids and pancreatiis in adults.
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Pancreatic trauma
Sits in front of vertebra so can get injured in blunt trauma. Integrity of duct is important. Delayed complication is pancreatic fistula followed by abscess formation. Imaging may be subtle - focal enlargement of pancreas. Low attenuation separating two portions of enhancing pancreas is laceration not contusion. Panc trauma in kid too young to ride a bike think NAI. Panc duct injury need MRCP or ERCP
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Acute pancreatitis
Gallstones and EtOH make up 80%. Others include ERCP, medications, trauma (most common in kids), panc ca, infectious, hypercalcaemia, hyperlipidemia, autoimmune, divisum, groove, tropic and parasite. Prognosis estimated with Balthazar score. Mild (no necrosis), severe (necrosis). Once necrosis and infected, high mortality rate. NO NECROSIS <4 weeks = acute peripancreatic fluid collection >4 weeks = pseudocyst NECROSIS <4 weeks = acute necrotic collection >4 weeks = walled of necrosis VASCULAR COMPLICATIONS Splenic and PV thrombosis (isolated gastric varices can be seen) Pseudoaneurysm of GDA and splenic a NON VASCULAR COMPLICATIONS Abscess and infection. Gas is characteristic sign of infected collection Inflammed pancreas hypoechoic on USS
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Panc divisum
Major duct of Wirsung drains to inferior of the two duodenal papilla. Minor duct of Santorini drains to superior of the two duodenal papilla. Santorini is smaller and drains superior DIVISUM Most common anatomic variant of pancreas. Occurs when main portion of pancreas is drained by minor or accessory papilla. Increased risk pancreatitis.
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Chronic pancreatitis
Result of prolonged inflammatory change leading to irreversible fibrosis. Acute doesnt have to lead to chronic and chronic can still have bouts of acute. Most common causes still EtOH and gallstones, now making 90% EARLY Low T1 signal. Delayed enhancement. Dilated side branches LATE Small/atrophic. Pseudocyst formation. Dilatation and beading of pancreatic duct with calcifications
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Chronic pancreatitis (CP) vs cancer
CP Dilatation is irregular. Duct <50% AP gland diameter CANCER Dilatation is usually uniform. Duct >50% of AP gland diameter
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Uncommon pancreatitis
AUTOIMMUNE IgG4. Responds to steroids. No duct dilatation, no calcs. Sausage pancreas. GROOVE Looks like panc head Ca but not duct dilatation. Duodenal +/- CBD strictures/stenosis 50%. SOft tissue within pancreaticoduodenal groove. TROPIC Young age, malnutrition. Increased risk adenocarcinoma. Multiple large calculi in dilated duct. HEREDITARY Young age. Increased risk adenocarcinoma. SPINK-1 gene ASCARIS Most common parasite. Worm may be seen in dilated duct.
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IgG4
``` Autoimmune pancreatitis Retroperitoneal fibrosis Sclerosing Cholangitis Inflammatory Pseudotumour Riedels Thyroiditis ```
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Cystic panc lesions
PSEUDOCYST By far most commonly inflammatory pseudocyst from acute or chronic pancreatitis SIMPLE CYSTS True epithelial lined cysts. Syndromes such as VHL, PCKD and CF
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Grandmother, mother, daughter
SEROUS CYSTADENOMA. Grandmother lesion in head of pancreas ('grandmother is head of the house'). Benign, heterogenous mixed density multiple small cysts <2cm resembling a sponge. 70% in panc head (mucinous almost always in body/tail). Does not communicate with panc duct. 20% central scar with or without central calcs. Rarely unilocular but when you see unilocular with lobulated contour should think macrocystic serous cystadenoma subtype. Association with VHL MUCINOUS CYSTADENOMA Mother lesion, women in 50s. Premalignant and need resection. In body and tail. No communication with panc duct. 25% peripheral calcs. Typically unilocular. When multilocular, cytic spaces are >2cm SOLID PSEUDOPAPILLARY TUMOUR OF PANCREAS Daughter lesion. Low grade malignant tumour in young females 30s. Large at presentation, predilection for tail and has thick capsule. Progressive fill in of solid portions.
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Intraductal Papillary Mucinous Neoplasm IPMN
Mucin producing tumours arising from duct epithelium. SIDE BRANCH Common, meaningless. SMall cystic mass in head or uncinate. Can cause duct enlargement if lots of mucin. <3cm usually benign MAIN BRANCH Diffuse dilatation of main duct. Can see atrophy of gland with dystrophic calc mimicking chronic pancreatitis. Much higher chance of malignancy than sidebranch. All cnsidered malignant and should consider resection CONCERNING FOR MALIGNANCY Main duct >10mm. Diffuse or multifocal involvement. ENhancing nodules. SOlid hypovascular mass
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Cystic panc lesion summary
MAIN BRANCH IPMN Bad one. Malignant potential SIDE BRANCH IPMN Common one. Much less malignant potential. Head/uncinate. Communicates with duct. SEROUS CYSTIC Grandma. benign. Microcystic with central calcifications. MUCINOUS CYSTIC Mother. Premalignant. Body/tail 95%. Unilocular with thick septations. SOLID PSEUDOPAPILLARY Daughter. Solid with cystic parts, enhances like hemangioma. Capsule.
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Ductal adenocarcinoma
Hypovascular. Enlarged GB with painless jaundice. Migratory thrombophlebitis (Trousseau's syndrome). Peak incidence 7th or 8th decade. Smoking is strongest RF. 2/3 of these are in panc head. Double duct sign with obstruction of CBD and MPD. Hypoenhancing mass, poorly demarcated, low attenuation.MRI low T1 signal. Assess SMA and coeliac axis which if involved make it unresectable. If GDA involved thats ok as its resected in Whipples. Tumour marker is CA19-9. Hereditary syndromes include HNPCC, BRCA, Ataxia telangiectasia, Peutz Jeghers. Wide duodenal sweep or inverted 3 on barium.
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Periampullary tumour
Originating within 2cm of major papilla. Can be cancers of distal CBD, pancreas or duodenum. DIfficult to differentiate from panc adeno. MRCP/MRI is study of choice. Increase incidence of ampullary carcinoma in Gardners syndrome.
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Islet cell/Neuroendocrine
NETs uncommon tumour of pancreas. Hypervascular with brisk enhancement in arterial of pancreatic phase. Non functional or functional and then divided into what hormone they make. Associated with MEN 1 and CHL. INSULINOMA Most common 75%. 90% benign, solitary and small <2cm. GASTRINOMA Most common with MEN 1 but second most common overall. Malignant 30-60%. Increased gastric acid output and ulcers. Zollinger Elison syndrome. Gastrinoma triangle is 90% of gastrinomas and is: Superior: junction of cystic duct and CBD Inferior: D2/D3 junction Medial: start of body of panc NON FUNCTONAL 3rd most common. Malignant 80%. Large with calc and metatstatic at time of diagnosis.
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Intrapancreatic accessory spleen
Possible to have panc mass which is just piece of spleen. Post traumatic splenosis. Follows spleen on all sequences, dark T1, bright T2. Tiger striped mass on arterial phase. Nuc med sulfur colloid or heat treated RBC
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Whipples
RESECT Panc head, duodenum, gastric antrum, GB. JOIN Jejunal loop brought up to RUQ for gastrojejunal, choledocojejunal/hepaticojejunal and pancreaticojejunal anastomosis. COMPLICATIONS Delayed gastric emptying and panreatic fistula. Both clinical diagnoses. Wound infection third most common
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Panc + renal transplant
Pancreas transplant (usually with renal transplant) is established therapy for severe T1DM. Often complicated by renal failure. Cause of graft failure usually acute rejection. May get splenic vein thrombosis. Venus thrombois smore common than arterial. Susceptible to pancreatitis. Shrinking transplant is buzzword for chronic rejection
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Normal spleen
Adult size by age 15. Red and white pulp makes tiger striped appearance on arterial phase. Red pulp filled with blood. SPlenic artery is end vessel with minimal collaterals - occlude and get spleen infarct. Pathology is congenital, acquired or mass. Most things with spleen are benign with exception of lymphoma and rare primary angiosarcoma MRI T2 bright, T1 dark, restricts diffusion.
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Accessory spleen
Very common. Sulfur colloid could be used to differentiate from enlarged pathologic LN. If prior splenectomy with residual splenules, these can enlarge and mimic mass.
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Wandering spleen
Wanders off into unexpected location. Laxity of peritoneal ligaments holding spleen, associated wth intestinal malrotation. Unusual locations can set up spleen for torsion and infarction. Chronic partial torsion can lead to splenomegaly or gastric varices
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Splenic trauma
Most common solid organ injured in trauma. Spleen holds about a unit of blood so can be life threatening. Needs to be done in PV due to tiger striped appearance on arterial.
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Splenosis
Occurs post trauma where smashed spleen implants and recruits blood supply. Multiple spherical nodules typically in peritoneal cavity of upper abdomen. Reported in 40-60% trauma. Sulfur colloid or heat treated RBC to confirm.
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Gamma Gamna bodies
Siderotic Nodules. Small foci of haemorrhage in splenic parenchyma usually associated with portal HTN. T2 dark. Gradient most sensitive.
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Sarcoidosis
Disease of unknown aetiology resuting in noncaseating granulomas which form in various tissues of body. Spleen involved 50-80% with splenomegaly. Aggragates of granulomatous splenic tissue may appear as discrete hypodense nodules. Gastric antrum most common site in GIT
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Peliosis
Rare. Multile bood filled cyst like spaces in a solid organ - usually liver (peliosis hepatitis). In spleen usually also liver. Aetiology not known. For MCQ, women on OCP or men on anabolic steroids. People with AIDS and renal transplants. People with Hodgkin lymphoma. Asymptomatic but can rupture spontaneously.
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Splenic artery aneurysm
Most common visceral arterial aneurysm. Pseudoaneurysm can occur in trauma or pancreatits. Incidence higher in women childbearing age and in women with >2 pregnancieis. Sacullar mid to distal artery. Fix when 2-3cm. Dont call hypervascular pan mass and biopsy.
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Splenic vein thrombosis
Frequently occurs as result of pancreatitis. Can also be in diverticulitis or Crohns. Can lead to isolated gastric varices.
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Spenic infarction
Number of conditions. Sickle cell. Wedge shaped peripheral low attenuation defect.
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Splenic infections
Most common is histoplasmosis with multiple rounded calcs. Spennic TB can have similar appearance. Calcifided granuloma may also be brucellosis which is solitary and large. Immunocompetent may get splenic abscess usually from aerobic organisms. Salmonella most common. Immunocompromisd get unusual organisms such as fungi, TB, MAI, PCP with multiple microabscesses
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Splenic size
``` SMALL Sickle cell Post radiation Post thorotrast Malabsorption syndromes UC and Crohns ``` ``` LARGE Passive congestion (heart falure, portal HTN, splenic vein thrombosis), Lymphome Leukemia Gauchers ```
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Feltys syndrome
Abnormality of granulocytes with: | Splenomegaly, rheumatoid arthritis, neutropenia
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Splenic cysts
POST TRAUMATIC Pseudocysts, most common cystic lesion in spleen. Secondary to infarction, infection, haemorrhage or extension from pancreatic pseudocyst. EPIDERMOID CYSTS Second most common. Congenital. Slow growing ften around 10cm when diagnosed. Can cause symptoms if large enough. Solitary 80% time and have peripheral calcs 25% time. HYDATID/ECHINOCOCCAL CYSTS 3rd most common. Parasite echinococcus Granulosus. Hydatid cysts consist of spherical mother cysts and often have daughter cysts. Internal septation and debris often referred to as hydatid sand. Waterlily sign when detachment of endocyst membrane resulting in floating membranrs.
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Further benign splenic masses
HEMANGIOMA Most common benign neoplasm. Smooth, well marginated and demonstrates contrast uptake and delayed washout LYMPHANGIOMA Rare. Most occur in childhood. May be solitary or multiple, most subcapsular. HAMARTOMA Rare. Hypodense or isodense with moderate hetergoenous enhancement.
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Mlignant splenic masses
Most things in spleen are benign. If malignant, likely vascular ANGIOSARCOMA Aggressive with poor prognosis. Poorly defined area of heterogeneity or low density in an enlarged spleen. Can contain necrosis and can rupture. Poor contrast enhancement. Post thorotrast. LYMPHOMA Most common malignant tumour of spleen, usually as minfestation of systemicdisease. Splenomegaly most common finding. Can get discrete nodules. METASTATIC DISEASE Mets to spleen is rare. Usually common things like breast, lung and melanoma. Melanoma most common.