MCQs Flashcards
Small bowel carcinoid
Calcifies in 70%
40% are in small bowel, mostly in terminal ileum > rectum > appendix
Take up octreotide - 15% don’t
Otherwise take up MIBG
Potentially malignant
Enterochrommafin cells, crypts of Leiberkuhn
(Pulmonary from Kulchitsky cells)
More common in small bowel than primary adeno in small bowel
Solid yellow tan
Size relates to malignant potential
And to met incidence - <1cm 2%, >2cm 85%
Xanthogranulomatous pyelonephritis
Chronic granulomatous pyelonephritis
Associated with staghorn calculus
Also pelvic contraction (with pelvicalyceal obstruction), perinephric infolvement, and multiloculated appearance.
Foamy macrophages, plasma cell, lymphocytes, PNLs, giant cells
May produce yellowish nodules, confused with RCC
E. coli and proteus most common (note E coli usually urease negative)
Female predominance 2:1 (presumably as higher rates of UTI)
Fatty infiltration
Hypoechoic infiltration of soft tissues
Rim enhancement on CT
UC v Crohns
Toxic megacolon more common in UC Crohns 10% colon involved Crohns skip lesions UC male predominant Perianal not common in UC, but is in Crohns Creeping fat Crohns Gallstones common in Crohns PSC more common in UC Erythema nodosum and pyoderma gangrenosum Apthous ulcer and Cobblestoning - Crohns Crypt abscess and pseudopolyps - UC Collar button ulcer - UC
Linear ulcer mesenteric border almost pathognomonic of Crohns
Serous cystadenoma pancreas
Central calcification Numerous small cysts Oligocystic varian in 10% Elderly Benign Associated with VHL Favour pancreatic head
Hyperechoic on ultrasoun.
Mucinous cystadenoma of pancreas
Younger Uni / multilocular Usually body or tail (head in 20%) Peripheral calc Elevated CEA, CA19-9 Malignant or premalignant
Cholangiocarcinoma
Typically obstructs bile ducts Progressive enhancement - early rim, with patchy central fill in and delayed (different enhancement pattern to HCC) Capsular retraction (characteristic) Klatskin - periductal infiltrating 1 - distal to confluence (i.e. Common hepatic duct) 2 - involves confluence 3 - involves left or right duct 4 - involves both ducts 90% are extrahepatic
DWI peripheral hyperintensity, target pattern, favours cholangiocarcinoma over HCC
Haemachromatosis
Iron deposits in liver
Later in pancreas
Not in spleen
Diffuse low T2 signal in liver
Prostate cancer
70% peripheral
Primary indication for MRI is to determine capsular extension if biopsy proven
May also be used when biopsy negative but persistent raised PSA
TR USS mainly to guide biopsy - otherwise poor
Mostly hypoechoic
Low T2 in normally high signal peripheral zone
Dynamic contrast enhancement can also be used - early enhancement with washouy
19-30% have normal PSA - need PSA >40 for bone mets
Rarely causes haematospermia
MR spectroscopy - increased choline and decreased citrate
Focal smooth thickened small bowel folds
Radiation in differential
Pancreatic ca resectability
CT good at prediciting unresectability
If tumour surrounds SMA or coeliac axis >180, unresectable (T4, stage 3. T3 if exends beyond pancreas but doesn’t surround vessels)
Rectal cancer staging
Stage 1 is T1 or 2
Stage 2 is T3 or 4
Stage 3 has nodes, 4 mets.
T1 Submucosa, T2 muscularis propria, T3 through muscularis into subserosal or non-peritonealised tissues, T4 invasive of organs/structures or visceral peritoneum
N1 1-3 nodes
N2 4 or more
Colon cancer staging
T1 submucosa
T2 muscularis propria
T3 through muscularis into subserosa or non-peritonealised tissues
T4 through visceral peritoneum or invading
N based on number of nodes - 1 1-3, 2 4 or more
Dukes A mucosal B muscularis propria C lymph nodes D mets
Anomalous biliary drainage
Most common is right posterior duct into left hepatic duct above confluence
Renal artery stenosis
Atherosclerosis involves proximal artery
FMD involves distal artery
PSV > 1.5 in transplant indicates stenosis
> 3.5 renal artery to aorta ratio
150cm/s if insonation <60 degrees, 180cm/s for >70
2:1 stenotic:poststenotic
Intraparenchymal RI >0.8
Intraparenchymal acceleration >0.07s
(RI may be increased in obstruction)
Cerebriform appearance of small bowel
Shock bowel
WDHA syndrome
Watery diarrhoea, hypokalaemia, anchlorhydria
VIPoma
Gastrinoma
10-15% occur in duodenum
In ZES and MEN1, usually multiple and in duodenum, <5mm, 75% in D1
Gallstones
Increased risk in chronic haemolysis (pigment stones)
Increased risk in Crohns disease - malabsorbed bile salts (TI) alter bilirubin reasorbtion (large bowel).
Barretts oesophagus
Reticular mucosal pattern in distal oesophagus on barium swallow (most sensitive finding)
Columnar (intestinal) metaplasia - need Goblet cells
Solitary rectal ulcer syndrome
Misnomer
35% solitary, 22% multiple, 43% no ulcer
Benign abnormality of rectal mucosa from straining - invaginates into lumen
Marked muscularis thickening
Failure of anorectal angle to open, incomplete emptying, rectal prolapse
May have inflammatory polyp (inflamed and elevated mucosa surrounded by granular muscosa)
Menetriers
Idiopathic hypertrophic gastropathy Bimodal - <10, 30-60, peak 55 Male predominant Fundus, relative antral sparing Differential lymphoma, other gastritis Clinical triad achlorhydria, hypoproteinaemia, oedema
Strongyloidiasis
Ulceration and stricture (stenosis) of D3 and 4, rigid pipestem
Dilatation of proximal duodenum with oedematous folds
Helminth parasite
Via skin, lung via lymphatics, then ascends and swallowed.
Can cause a colitis in immunocompromised
Amoebiasis
Protozoan
May cause toxi megacolon
Loss of haustral pattern
Collar button ulcers
Apthous ulceration
Right colon and caecum > flexures > rectosigmoid
May mimic Crohns, but spares TI unlike Crohns, TB
Invades crypts, burrows into tunica propria
Amyloid
Primary
Duodenum > stomach > colon, rectum > oesophagus
May cause linitis plastica, or submucosal mass
Can cause GI bleeding
Diabetes
Can cause gastric dilatation secondary to autonomic neuropathy
Adenomyomatosis
Localised, segmental, or diffuse Localised often in fundus Segmental often in waist Not premalignant Gallstones in 25-75%
TB peritonitis
Dense ascites - wet peritonitis
Omental caking - fibrotic peritonitis
Mesenteric caking, fibrous adhesions, caseous nodule - dry peritonitis
Buscopan, contraindications
Anticholinergic Closed angle glaucoma Tachyarrythmias Megacolon Myasthenia Urinary retention Bowel obstruction Paralytic ileus Urinary retention
Cathartic colon
Prolongued stimulant laxative use Neuromuscular incoordination Right predominant Absent haustration Patulous Ileocaecal valve DD UC - recutm spared, no pseudopolyps. no ulceration No increased cancer risk
Acanthosis nigricans
Skin changes
Mostly from insulin resistance, obesity
May be due to malignancy GI - gastric, HCC, lung, uterine
Coeliacs
Decreased jejunal folds, increased ileal
Low density nodes
Increased risk of T cell lymphoma, small bowel adeno, oesophageal SCC, HCC, colorectal ca, breast
Healing of villous atrophy reduces somewhat the lymphoma risk, but an increased risk remains
Antigliadin antibody 10-20% false positive
EMA 100% specific, 90-95% sensitive
Transglutaminase antibody 98% specific, 95% sensitive
Colovaginal fistula
Diverticulitis most common cause
Oesophageal rings
A transient muscular contraction
B squamocolumnar junction
C diaphragm crura
Afferent loop syndrome
Obstruction to upstream limb of side to side gastrojejunostomy
May have bilious vomiting
Causes: anastomotic kinking, radiation stricture, recurrent tumour
Recurrent rectal Ca
Distinguish from scar by PET
CEA
Up in 60-90% of colorectal Ca
Also other malignancies - breast, lung, bladder, pancreatic, thyroid
And non malignant - smoker, PUD, IBD, pancreatitis, ccirrhosis
Scleroderma small bowel
Hidebound bowel - bunching and crowding of folds (which aren’t thickened - also seen in sprue [coeliacs and tropical sprue]) [not the same as stack of coins, from intramural haematoma, where folds are thickened - coagulopathy and vasculitides]
Antimesenteric sacculations / pseudodiverticula
Dilated duodenum, jejunum
Prolonged small bowel transit time
Also affects colon in 40-50% with pseudosacculations, loss of haustra, marked dilatation, stercoulceration from retained faeces
Women, 30-50 (3xmen)
Arthropathy fingers, wrists ankles 70-97%
Oesophageal involvement 80%
Respiratory histologically in all, but only minority / 25% have symptoms
UIP or NSIP, pulmonary artery HTN
Dilatation of distal 2/3 of oesophagus
Fusiform stricture 4-5cm above GE junction
High risk of adenoCa
Progression to Barrets
Small bowel in 60%
Dilatation which can be massive
Crowded folds / hidebound bowel
Antimesenteric pseudosacculations
Peutz Jager
Hamartomatous polyps
Increased risk of GIT carcinoma, breast, adenoma malignum (an adenoCa of cervix)
Pancreas, ovaries, testes, lung, uterus
Polyps mostly small bowel
Mucocutaneous pigmentation
Continuous smooth muscle core with the muscularis differs from other hamartomatous polyposes. The hamartomas are non-neoplastic.
GI lymphoma
Gastic > small bowel esp ileum > proximal colon > distal colon > oesophagus and appendix rare
Ileum most common small bowel site (as mentioned above)
Appendicitis in pregnancy
Increased risk of perforation
Probably because of delays in diagnosis and treatment
Perianal fistula
1 - linear intersphincteric
2 - interspincteric with abscess or secondary fistulous tract
3 - trans-sphincteric
4 - trans-sphincteric with abscess or secondary fistulous tract in ischioanal or ischiorectal fossa
5 - supralevator or translevator disease
Gastric ca risk
Chronic atrophic gastritis
Partial gastrectomy - bilroth 2 > 1
Whipple disease
Thickened (fine) nodular folds (swollen villi) in distal duodenum and jejunum. Normal calibre bowel. Infiltration by macrophages, and lymphatic obstruction.
Low attenuation nodes
Hepatosplenomegaly, ascites
Sacroiliitis
No ulceration. Normal transit time. No rigidity of folds.
Wild mucosal pattern.
Bilroth
1 - gastroduodenostomy - direct attach
2 - side to side anastomosis from gastric to jejnum. Afferent limb (biliopancretic limb) proximal to anastomosis, efferent limb distal
Biroth 2 has higher gastric ca risk than bilroth 1
Hepatorenal syndrome
Rapid deterioration in renal function in patients with cirrhosis or fulminant hepatic failure
Liver failure causes altered blood flow to kidneys
Medullary nephrocalcinosis
20x more common than cortical Hypercalcaemic, hypercalcuric HPT, MSK, RTA Vit D, sarcoid, cushings, mets, myeloma Renal TB, infection Sickle cell Renal papillary necrosis Durgs - furosemide
Upper pole duplex
Ectopic and obstructs
Can be into seminal vesicles
May present with epididymo-orchitis
Bilateral increased renal size
TB, leukaemia, RTA, HUS
Fish-hooking distal ureters
Prostatomegaly
Medial deviated ureters
AAA, retrocaval ureter, retroperitoneal fibrosis (proximal)
Iliopsoas hypertophy
Iliac adenopathy
Iliac aneurysm
Hutch diverticulum (VUJ)
Following AP resection and retroperitoneal lymph node dissection
Pelvic lipomatosis
Rim nephrogram
Perfusion maintained around rim of devasculrised kidney from capsular vessels
Develops >8 hours
Fluid collections post renal transplant
Immediate post-op - haematoma
1-2 weeks - urinoma
3-4 weeks - abscess
2 months and beyond - lymphocoele
Papillary v clear cell RCC
Papillary enhances less Papillary hypo T2, clear cell hyper T2 Clear cell most common Papillary better prognosis VHL - clear cell Dialysis associated - papilary Smoking major RCC risk factor
RCC risk factors - smoking, obesity, cyclophosphamide, dialysis cystic disease (mostly papillary)
Renal vein thrombosis causes, child
Dehydration Sepsis Sickle cell Polycythaemia Maternal diabetes Indwelling umbilical venous cathether
Renal vein thrombosis causes, adult
Nephrotic synd SLE Amyloid Glomerulonephritis Diabetes Renal sepsis Renal tumour Trauma
Testicular microlithiasis associations
GCT (debatable increased risk) Cryptorchidism Klinefelters Downs Male pseudohermaphraditism
Testis teratoma
In child benign
In adult malignant
Tend to occur in younger age group than seminoma
PSA for bony mets
>
- <20 is uncommon
85% NPV for prostate Ca of PSA <4
Testicular radiosensitivity
Seminoma senstive
Rest not
NSGCT more aggressive, worse prognosis
Bosniak
3 - thick enhancing septa, remove
4 - clearly malignant
1-3% of cysts calcify
3 - 50% chance of malignancy
Thin <1mm septa normal - 2
Epididymal tumour
Adenomatoid most common
Slow growing mesothelial neoplasm
2nd-4th decade
Tail particularly
Renal TB
Normal CXR in 50%
Moth eaten calyx - necrotizing papillitis
HUS
Increased cortical echogenicity from acute cortical necrosis
In differential for bilateral enlarged kidneys
MORE DESCRIBING THE CONDITION
Indinavir stone
Renal stone not seen on any modality if pure
HIV treatment
Oxalate stones
Crohns without ileostomy increases risk - fat malarbsorption, so more bound calcium by fat, so less oxalate bound by calcium
Radiopaque
HIV nephropathy
Normal kidney size
Carney’s triad
GIST, pulmonary chondroma, extra-adrenal paraganglioma
Phaeo
10% have speckled calc
10% malignant
Familial 10% - VHL, NF1, MEN2, Sturge-Weber
10% extra-adrenal - these are more likely to be malignant
10% bilateral
Extra-adrenal more likely to be malignant
T2 hyper to liver (unlike adenoma which are similar to liver) (markedly hyperintense - lightbulb sign)
Avid enhancement, may washout
Calc in 7% (cortical carcinoma in 30%)
MIBG
to detect phaeo mets
taken up by small bowel carcinoid
Transjugular liver biopsy
Good when bleeding risk, as minimised
PBC
Has adenopathy more than other causes of cirrhosis
AMA (antimitochondrial antibody) sensitive and specific
Middle aged women
Chlonorchis sinensis
Chinese liver fluke
Intrahepatic calculi
Solid bening hepatic
Haemangioma most common
Then FNH
Budd-Chiari cause
Idiopathic 2/3 (or 1/3 depending on source)
Thrombotic - pills, pregnancy, PCV, PNH paroxysmal nocturnal haematglobinuria
Vessel wall injury - radiation, chemo/immunosupression in BMT patients, jamaican bush tea
Tumour extension - RCC, HCC, adrenal, leimyosarc of IVC
Treat - medical, thrombolysis, angioplasty / stent, TIPS,
Caudate hypertrophy (in some - not seen in majority on NM), spider web hepatic venous collaterals
VHL pancreatic associations
Cysts, cancer, serous cystadenoma, islet cell tumours (tend to be non-functioning), NOT MUCINOUS
Choledochal cysts class
1 fusiform dilatation extrahepatic 2 diverticulum 3 within duodenal wall 4 multiple 5 intrahepatic only - Caroli disease
Bile stasis
Cholangitis, bilirubin stones, liver abscesses
Anabolic steroids
Can cause pure cholestasis and NASH
Also risk factor for heaptic adenoma
Hepatic adenoma
Heterogeneous (enhancement and ultrasound)
OCP, anabolic steroids, glycogen storage disease
Negative sulphur colloid and hepatobiliary contrast MR
Commonly T1 dropout
Fat or haemorrhage - may have calcium (5-10% in areas of old haemorrhage)
Can malignantly transform, haemorrhage, rupture
Less common than FNH, haemangioma
USS may show flat trace -perilesional sinusoids
TYPES:
.
Pancreatic endocrine tumours
2% MEN1
Also VHL, TS
Syndromic and non-syndromic tumours
Insulinoma > gastrinoma > glucagonoma, VIPoma, somatostatinoma
Vascular, may be cystic
10% of insulinoma malignant
Others around 75%
DD met RCC, splenule, solid serous cystadenoma
80% take up octreotide - gastrinoma best, insulinoma worst
70% of insulinoma <1.5cm, less than 1% extrapancreatic (gastrinoma ectopic 7-33%).
Mucinous cystadenoma pancreas
Peripheral egg-shell calc specific for malignancy
Chronic pancreatitis
Alcohol
2-4% get cancer
Pancreatic pseudocyst
10-20% of acute pancreatitis
Spontaneously resolve 25-40%
OCP use
Increases risk of HCC slightly
Peliosis hepatis
Blood filled cavities in liver
Steroids, OCP, tamoxifen, oestrogens
HIV AIDS, transplantation, haem/onc disorders, some infections - bartonella
Toxins
May haemorrhage, hepatomegaly, liver impairment
Hepatic pseudotumour
Young asian males
Associated with recurrent pyogenic cholangitis
Right lobe
Not typical imaging - biopsy or surgery required
More common in lung and orbit
Secondary sclerosing cholangitis
AIDS cholangitis
Or stricture from previous surgery, ischaemia
AIDS - cryptosporidium, CMV
Regenerative liver nodule
Non-neoplastic nodule in cirrhotic liver
If not cirrhosis, NRH
If iron, siderotic
Cirrhotic nodules range from benign regenerative to dysplastic to HCC
TIPS
Change in velocity >50cm/s relative to baseline may indicate significant stenosis
Flow should be 50-150
Also elevated maximum and depressed minimum
Biliary dilatation may be an acute complication - fistula
Contraindicated in RHF, pulmonary HTN, hepatopulmonary syndrome
Is a treatment for refractory ascites, Budd-Chiari, portal HTN / varices, hepatorenal syndrome, portal hypertensive gastropathy, hepatic hydrothorax, malignant compression of portal or hepatic veins
Contraindications: fulminant failure, encephalopathy, severe right heart failure, sepsis
(because 1 liver may not tolerate lack of portal nutrients, 2 more toxins may get to brain, 3 increased preload, 4 stent may get infected
Hypervascular liver mets
Renal, lung, breast, thyroid, carcinoid, melanoma, HCC, choriocarcinoma
Hyperechoic liver mets
Colon, RCC, carcinoid
Hypoechoic liver mets
Lung, breast, pancreas, lymphoma
Tamm-Horsfall protein
In urine, from renal casts in ATN
GI bleeding
0.5mL/minute to detect on angiography
0.1mL/minute on muclear medicine
Diverticula in right colon are more likely to bleed than on the left - 3x
GI ischaemia
If good collaterals, so doesn’t perforate bowel, may result in a stricture
SMA occlusion:
Embolic 60%
Thrombosis superimposed on atherosclerosis 30%
Aortic dissection
Embolism - 15% at origin, 50% just distal to middle colic artery
Venous thrombosis 5-15% of cases
Haematogenous small bowel mets
Prediliction for antimesenteric wall
Testicular cysts
Seen on USS in 10%
Cushings
5% from carcinoma, most in children (66%)
20% from adenoma (or carcinoma) secreting cortisol
80% from increased ACTH production by a tumour - pituitary mostly, but also ectopic - small cell lung, carcinoid, pancreatic neuroendocrine, phaeo, ovarian benign
Rarely ACTH independent hyperplasia
Adrenal mass
Large size and calc suggest malignancy
Carcinoma calc 30%, phaeo 10%
Adrenal hyperplasia
Occurs more commonly in malignancy
Paraduodenal hernia
The most common type of internal hernia
Left more common than right
Failure of fusion of ascending / descending colon mesenteries
R is associated with small bowel malrotation
Pancreatitis, SLE
May be secondary to vasculiti, small vessel ischaemia, immune complex deposition or a combination
Most common splenic benign lesion
Haemangioma
CF
Increased risk of colon, pancreatic, biliary malignancy and lymphoma
PNH
Paroxysmal nocturnal haemoglobinuria
A haemolytic anaemia - complement destroys rbcs.
May be primary, or secondary to another bone marrow disorder
26% have red urine in morning
May cause thrombosis - legs (DVT), hepatic veins (Budd-chiari) portal vein, mesenteric veins, cerebral
Colonic lipoma
Benign, caecum and ascending colon, don’t degenerate
Achalasia
1000x risk of adenocarcinoma
(also increased risk of SCC)
Vestibule is the region of the lower oesophageal sphincter which fails to relax
5% risk of perforation from pneumatic dilatation
May have nocturnal reflux and aspiration
Spindle cell ca oesophagus
A type of SCC
Relatively little obstruction
AIDS abdominal manifestations
MAI infection - bowel dilatation
Toxic megacolon (pseudomembranous colitis)
Perirectal abscesses, lymphoma
Reactive hyperplasia is the most common cause of lymphadenopathy
Kaposi shows strong enhancement
Schistosomiasis
Bladder wall calcs, can lead to SCC
Wolman disease
AR
Deposition of fat in various organs
May have bilateral enlarged calcified adrenal glands, hepatosplenomegaly, and enlarged nodes
Hydatid cyst
Daughter cyst in 70%
Echinococcus granulosa
Death of parasite implied by complete calcification
ADPKD
Do not invariably have liver cysts, but majority and increasing incidence with age Associations: Bicuspid valve Berry aneurysms HTN Diverticulosis Cranial dolichoectasia Multiple biliary hamartomas Aortic dissection Mitral valve prolapse Liver cysts 75% by 60 Seminal vesicle cysts 60% by 40 Pancreatic, prostate
Lipiodol
Taken up by HCC and normal hepatocytes, not cleared by HCC so do delayed scanning
Pancreatic duct
3mm young, 5mm elderly
Divisum in 5%
Caroli disease
Stones, cholangiocarcinoma, bacterial cholangitis, renal cystic disease associations
Multifocal cystic dilatation (sacular often - recurrent pyogenic cholangitis gives fusiform dilatation) of intrahepatic bile ducts
Central dot sign of enhancing portal radicles within the dilated bile ducts
Hepatic attenuation
Decreased in Wilsons as steatosis (can be increased from Copper, but not majority)
Increased in amiodarone, gold, iron (haemochromatosis, haemosiderosis), glycogen storage disease
CT cholangiography
No good if serum bilirubin 3x normal because impaired excretion of contrast agent
95% sensitive if bilirubin normal
FNH
20% will be decreased uptake on sulfur colloid. 33% have increased uptake.
Adenomas are photopenic on sulfur colloid
Chagas
Mega oesophagus or colon in 1/3
Also myocarditis
Dermatomyositis
Disordered peristalsis of oesophagus
Infectious oesophagitis
Candida: mucosal nodularity and longitudinal plaques, may be shaggy in severe cases (also granularity, fold thickening)
CMV: one or more large ovoid ulcers (although can have multiple small superficial ulcers, more like HSV). A giant ulcer is more suggestive of CMV. May be indistinguiable from HIV, HSV
Adrenal adenoma
Chemical shift MR most accurate in differentiating from mets.
Absolute washout >60%
Relative washout >40%
T2 similar to liver, whereas phaeo has higher T2
Adrenal cortical carcinoma
Associated with congenital hemihypertrophy (Beckwith Wediedeman
And LiFraumini, Carney complex (not the same as Carney Triad), MEN1
30% calcify
Large, extend into liver, IVC, renal vein
May look identical to phaeo on imaging
Omental infarct
90% right sided
Appendicitis diameted
> 6mm
Portal HTN ultrasound
Portal vein >13mm (non-specific)
Flow reduced <35cm/s
Defined as pressure >12mmHg or portosystemic gradient >5mm
CBD US
<6mm, +1 per decade over 60
Mag3 renogram T1/2
<10 normal, >20min obstructed (after lasix)
Schatzki ring
Symptomatic B ring (mucosal squamocolumnar junction)
Symptomatic if <13, sometimes if 13-20mm
Renal stone, size, pass
4mm will pass, 8mm won’t, 4-8 variable
Risk of colon malignancy with polyp size
<5mm, <1%
5-9mm, <1-2%
10-20mm, 10%
>20mm 40-50%
Colon cancer
5% synchronous
55% rectosigmoid. 20% caecum / ascending (including IC valve), 10% transverse, 5% descending
Asbestos is a risk factor
IBD genetics
10% risk in 1st degree relatives
Cronkite Canada
Non-hereditary hamartomatous polyposis
Throughout GI tract
Cutaneous manifestations - pigmentation, alopecia, onychodystrophy
Cowden
Hamartomatous polyps
AD
Polyps mostly skin and mucosal membranes, but also GI tract
Follicular thyroid cancer
Skin, oral, breast and uterine malignancy
Lhermette-Duclos
Fibrocystic disease of breats, thyroid adenomas, glycogenic acanthosis
Oesophageal ulcer, table
Solitary large flat
Oesophageal cancer, gross morphology
Polypoid/fungating (most common)
Ulcerating
Infiltrative (obtuse margins)
Superficial spreading / varicoid - thickened nodular folds
Zollinger Ellison
FUSED Folds (thickened) Ulcers Secretions Edema Diarrhoea
Villous adenoma, clinical
Can secrete potassium and protein and cause hypokalaemia and hypoproteinaemia
Eosinophilic gastroenteritis
Unknown aetiology
Common to have atopy
Peripheral eosinophilia
Infiltration of any or all layers of gut wall by eosinophils (one source talked about mucosal and muscular types)
Gastric antrum and proximal small bowel common
Fold thickening and nodularity - may give a cobblestone appearance
Steroids
Usually middle age
GVHD
Skin, small bowel (and remaining GI tract), and liver most common
Host immune system activates donor T cells, causing inflammatory cascade
GI mucosal fold thickening, may lose folds in ileum
May have strictures and dilatation proximal to these
Mastocytosis
Mast cell proliferative neoplasm
Diffuse bony sclerosis
Small bowel diffuse nodular irregular thickened folds, sand like nodules (from mast cell / other cell infiltration)
Scleroderma, oesophagus
Atonic distal 2/3 with patulous sphincter
Dysmotility leads to reflux, Barrets, lower oesophagus stricture, aspiration, candida
Women, 30-50 (3xmen)
Arthropathy fingers, wrists ankles 70-97%
Oesophageal involvement 80%
Respiratory histologically in all, but only minority / 25% have symptoms
UIP or NSIP, pulmonary artery HTN
Dilatation of distal 2/3 of oesophagus
Fusiform stricture 4-5cm above GE junction
High risk of adenoCa
Progression to Barrets
Small bowel in 60%
Dilatation which can be massive
Crowded folds / hidebound bowel
Antimesenteric pseudosacculations
Epididymitis
20-40% have orchitis
Can look like torsion
Renal calculi
RTA can cause calcium phosphate calculi
Most calcium containing stones have idiopathic hypercalcuira (or are on loop diuretics or acetazolamide)
Struvite (triple phosphage / magnesium ammonium phosphate stone)- urease bacteria (proteus, klebsiella, pseudomonas, enterobacter. Stones usually mixed with calcium so radiopaque
Uric acid e.g. gout (lucent - mildly opaque on CT)
Cystine e.g. metabolic cyteinuria (lucent - mildly opaque on CT)
Meds e.g. indinavir (radiolucent, HIV)
Crohns - malabsorbed fats bind calcium so calcium can’t bind oxalate, so oxalate stones. Oxalate is resorbed in the colon, so if Ileostomy, don’t have the same risk
Malacoplakia
Chronic granulomatous inflammation of bladder wall
Common in immunocompromised or chronic disease - AIDS, DM
E coli infection common
Michaelis-Gutmann bodies are histological hallmark - intracellular calcium inclusions
Multiple bladder masses or circumferential thickening, associated with reflux and ureteric dilatation (can commonly obstruct)
Can occasionally be locally aggressive
Medical treatment first line. Vitamin C included. Surgical options.
Gallium scintigraphy can detect clinically silent lesions
Renal cortical necrosis
May cause cortical nephrocalcinosis, with punctate / dystrophic calc.
Medullary, cortical nephrocalc mnemonics
And renal papillary necrosis mnemonic
Medullary - HAMHOP
Cortical - COAG
RPN - NSAID
Hypercalcuria/aemia Acidosis (RTA) MSK HPT Oxalosis Papillary necrosis
Cortical necrosis
Oxalosis
Alport syndrome (hearing loss, ocular abnormalities, haematuria, leiomyomas)
Glomerulonephritis (chronic)
NSAID Sickle cell Analgesics Infection (pyelo and TB) Diabetes and dehydration
Properitoneal fat strip
Anterior extension of the posterior pararenal space
Lost in: appendicitis, ruptured AAA
Perirenal abscess, plain film
Loss of renal outline Loss of psoas shadow Scoliosis, convex to side of abnormality Anterior displacement of descding duodeneum Loss of properitoneal fat strip
Intratesticular varicocele
Usually in association with an ipsilateral extratesticular varicocele
Ureteritis cystica
AKA pyelitis cystica (renal pelvis), cystitis cystica (urinary bladder), pyeloureteritis cystica
Multiple submucosal cysts in the ureters
Older women with recurrent UTIs
Perhaps increased TCC risk but probably relates to the underlying cause
?maybe associated with diabetes
Renal NM
DMSA tubular uptake (cortex) - scarring, differential of renal function
DTPA - GFR, filtered
Mag3 secreted, tubules, and glomerular filtration. Highly protein bound in serum. Accumulates in ATN
Renal transplant
Dilatation of collecting system without obstruction common in a normal transplant kidney
Vascular compromise in 1-2%
Increased renal size (oedema) may be first sign of rejection
Renal leukaemia
Hyperdense
Endodermal sinus tumour
Is a synonym for yolk sac tumour
Cholecystostomy
Can be complicated by bradycardia and hypotension
Hepatic haemangioma
F:M 5:1
T1 hypo, T2 hyper
Multiple in about 30%
Progressive fill in
Coursouviers law
Palpable enlarged gallbladder, with painless jaundice, cause is unlikely to be gallstones
Gallstones are formed over extended period of time, so get fibrotic gallbladder which cannot distend easily
Hepatoduodenal ligament
CBD anterior and right
Hepatic artery anterior and left
Portal vein posterior
Portal vein thrombosis
Reduced flow - cirrhosis, malignancy
Hypercoagulable state - V leiden, C, S, antiphosopho. Pregnancy, malignancy, drugs (OCP), dehydration
Endothelial damage - pancreatitis, ascending cholangitis, abdo surgery (actinomycosis in prev question)
Cholelithiasis
Haemolysis e.g. thalassaemia, sickle cell. Also Cirrhosis with hypersplenism. Wilson’s can thus cause via cirrhosis.
Cystic fibrosis - biliary cirrhosis
Cholesterol stones (>50% cholesterol) - 10%. Diet, weight loss, obesity, contraceptive Mixed (20-50%) - 80% Pigement sones - 10%, high bilirubin content from supersaturated unconjungate bilirubin. May have black sontes (cirrhosis, haemolysis, intestinal malabsorption e.g Crohns), or brown (bacterial, parastic infection e.g. clonorchis, and biliary stasis)
Haemachromatosis
Increased out of phase signal as not susceptible to T2* low signal
Multilocular cystic nephroma
Bimodal - 3month to 4 years, 75% male, and 40-60, mostly females
Benign
Multilocular cystic on imaging, encapsulated
Calc, haem and necrosis uncommon
Usually remove due to confusion as below
In adults, can look like a multilocular clear cell RCC
In children difficult to tell from cystic Wilms (1-11, peak 3-4)
MCDK is usually diagnosed antenatally whereas this presents later, plus have some normal kidney in this cf MCDK
Metanephric adenoma
Polycythaemia in 10%, from EPO
Benign, 40-60 peak but can be any age, F 2xM
Difficult to differentiate from other renal tumours
Calc in 20%
RCC
Calcify 30%
Clear cell T2 hyper
Papillary T2 hypo
Heterogeneous T1 - necrosis, solid, haemorrhage
Organ of Zuckerkandl
Small mass of chromafin cells by aorta
Highest concentration near IMA origin
Extends from near SMA down to bifurcation
Vas deferens calc
Diabetes most common Idiopathic / aging Chronic infection: TB Syphilis Shistosomiasis Gonorrhoea Chronic UTI
PSC
Strongly associated with IBD, esp UC
AIDS cholangitis indistinguishable
May have secondary to other cause e.g. surgery causing stricture
Strictures, dilatations, and divertulae of biliary tree
Increased risk of cholangiocarcinoma. Also HCC (as causes cirrhosis). And increased risk of bowel cancer (4x that of IBD without PSC, and 10x general population)
Associated with other IgG4 diseases.
PSC men 40, PBC young women, with high AMA sensitive and specific for PBC (PBC typically doesn’t have lots of bile duct signs)
Recurrent pyogenic cholangitis
Diagnosis of exclusion Intraductal pigment stones Stricutres and dilatations of ducts More common in SE asia E coli and Chlornochis (liver fluke) have been implicated by causation not understood
Haemochromatosis
T2* signal loss
Opposite to fat on in and out of phase imaging - ie higher on out of phase imaging
Spleen and bone marrow signal typically normal
Pancreatic signal only low if cirrhosis
Wilsons
Copper doesn’t affect MR signal
CT may be up (from copper) or down (as get fat deposition) or normal.
Changes of cirrhosis
HCC staging
Barcelona clinic liver cancer staging system
Also Milan criteria for liver transplantation
BCLCstaging
Incorporates: tumour extent (size, multiplicity, vascular invasion, nodes and mets), ECOG performance status (0 fine, 5 dead), and Child-Pugh score
0-A-D
The Child-Pugh score is an assessment of liver function in chronic liver diseases and incorporates bilirubin, Albumin, INR, ascites, hepatic encephalopathy
Renal cancer staging
TNM and Robson
T1 and 2 just in kidney 1<7cm, 2>7cm
3 extends into veins or perinephric tissue, but not beyond Gerota’s fascia or to ipsilateral adrenal gland
4
N1 regional nodes
M1 mets
Robson: 1 kidney 2 perinephric fat 3 veins or nodes 4 mets or invasion or organs/structures (This is similar to the Dukes staging of Bowel ca)
Mets are most commonly to: lungs, bone, lymph nodes, liver, adrenal, brain
Oesophageal cancer staging
T1 invades lamina propria, muscularis mucosa or submucosa
T2 invades muscularis propria
T3 invades adventitia
T4 invades adjacent structures, “a” resectable (pleura, pericardium, diaphtram) “b” unresectable (aorta, trachea)
N1 1-2 regional nodes
N2 3-6
N3 - 7 or moe
Gastric cancer staging
T stage identical to other GI malignancies
N the same as oesophageal
Pancreatic cancer staging
T mostly sized based, with 4 if SMA or coeliac axis involved - resectability not included in assessment
1 <2cm, 2 2-4cm, 3 >4cm
N same as bowel - number of nodes, 1 1-3, 2 4 or more
Retroperiteoneal liposarcoma types
Well differentiated (55%, low grade), myxoid (30%, mostly low grade), pleomorphic, round cell, and dedifferentiated (final 3 high grade)
Renal trauma grading
AAST american association for the surgery of trauma
1-5
1 - contusion or non-enlarging subcapsular haematoma
2 - <1cm
3 - >1cm but not to pelvis or collecting system
4 - Lac extends to renal pelvis or urine leak, or main vascular injury, or enlarging haematoma compressing kidney
5 - shattered or avulsed from vessels or ureter
Hepatic trauma grading
AAST 1-6
1 lac <1cm or subcap haem <10%
2 lac 1-3cm depth (<10cm long), haem <10cm, or subcam haem 10-50%
3 lac >3cm depth, haem >10cm or subcap haem >50% or ruptured haem
4 25-75% of a lobe or 1-3 segments
5 >3 segments in one lobe or >75% of one lobe, or major venous injury
6 avulsed
(1-3 similar to spleen but a bit different - 10cm rather than 5cm for haem)
Splenic trauma grading
AAST 1-5
1 Lac <1cm, subcap haematoma <10%
2 Lac 1-3cm depth, Haematoma <5cm, subcap haematoma 10-50%
3 Lac >3cm depth, Haematoma >5cm or subcap haematoma >50%, or ruptured haematoma
4 Lac involves vessles with major devascularisation >25%
5 shattered or devascularised
(1-3 similar criteria to liver but a bit different = 5cm rather than 10cm for haem)
Pancreatic trauma grading
AAST 1-5 1 minor contusion or lac 2 major but withoug duct injury 3 distal duct injury 4 proximal duct injury (right of SMV) 5 massive disruption of pancreatic head
Small bowel folds
.
Adrenal cortical v phaeo
ACC - large, calc in up to 30%, relative contrast retention, necrosis and haemorrhage. Liver mets tend to be hypervascular
Phaeo may look identical. Differentiated by histology, biochemistry, functional status
Phaeo calc in 10%
Phaeo tends to enhance a lot. May wash out.
Phaeo also large, and heterogeneous with necrosis and haemorrhage
Pancreatitis CT grading
.
Most common small bowel tumour
Leiomyoma (GIST)
Malignant: adeno then carcinoid then lymphoma then leiomyosarcoma
Small bowel lymphoma risk factors
Coeliacs
HIV / AIDS
H pylori
Post transplant
GIST
Stomach 70% Small intestine 20% Anorectum 7% Colon Oesophagus (oesophagus call tumours leiomyoma in general)
Phi angle
Normally between 4 and 58
Gastric band
Angle between vertical of vertebral column, and long axis of band
Splenic metastses
Melanoma Breast Ovarian Colorectal Gastric Lung
