Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Z3. GI FRCR 2A Primer > 3_primer_mankad_hoey_20150316195806 > Flashcards

3_primer_mankad_hoey_20150316195806 Flashcards

1
Q

Hepatic Artery Variants

A

50-60% from CHA via Coeliac axis, then CHA divides to proper HA and GDA10% CHA divides into RHA and GDA10% CHA divides into LHA and GDANormal HA velocity 30-60 cm/s; RI 0.6±0.06; continuous diastolic flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Portal Vein

A

Hepatopetal, non-pulsatile, mild respiratory variationFlow velocity 20-30 cm/sDiameter 12-14 mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hepatic Vein

A

Triphasic with respiratory and cardiac variationHV sampling occurs at its confluence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cirrhotic nodules

A

Regenerative (hepatocytes and stroma; not seen on US unless large; on CT are high attenuation if siderotic)Cirrhotic (regenerative nodules with surrounding fibrosis)Dysplastic (hepatic adenomas with areas of dysplasia; due to HBV and HCV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Imaging features of Cirrhosis

A

Decrease size of right lobe and medial left lobe, with caudate lobe hypertrophyMRI:Regenerative nodules: high T1W, low T2W;Dysplastic: high T1W, very low T2W, with post Gd enhancement;Neoplastic: arterial enhancement with PV washout; nodule-in-nodule on T2W (high T2W neoplastic within low T2W dysplastic nodule)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Haemochromatosis

A

Primary (AR) due to increased uptake of transferrinSecondary - erythrogenic, Bantu siderosis or transfusional (>30 units blood)CT - high attenuation liver with low attenuation PV branchesMR - Liver low T1W and T2W relative to muscle, with susceptibility on GRE; pancreas low late in disease, spleen normal in primary but low in secondary disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Liver Abscess

A

Cause: 80-90% bacterial, 5% amoebic, 50%), ofetn contain gas and 60-70 y/o peakAmoebic: due to entamoeba histolytica, usually 30-50 y/o, usually single, in peripheral right lobe and often >5 cmImaging: raised right hemidiaphragm, hypoechoic initally, then developing thick reflective wallCT signs specific to pyogenic abscess: Double target sign (enhancing wall with surrounding oedema), cluster sign (clustered abcesses)MR: Low T2W, high T2W, enhancing wall, low signal wall on T2W with surrounding perilesional oedemaNM: Uptake of sulphur colloid; Gallium taken up by pyogenic but not amoebic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hepatic Haemangioma

A

Commonest benign liver lesion (70 to 80%), usually 4 cm = giant cavernous haemangioma.Associations: FNH, HHT, Kasabach-Merritt Syndrome (Haemangioma and thrombocytopaenia).Supplied from hepatic artery, may rupture spontaneously.Usually hyperechoic on US, ± posterior acoustic enhancement, no flow on DopplerCT: low attenuation with early peripheral nodular enhancement, delayed centripetal fill in to maximal at 15 minutes.MR: Sharply defined, low T1W, very high T2W, central fibrous scar, similar enhancement to CT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

FNH

A

Second commonest benign liver lesion, usually right lobe, FCentral scar (containing AVM), usually on liver surface, non-encapsulated ± pedunculated,, very vascular, contains Kupffer cells, non-calcifiedUS: Homogeneously hyperechoic with hypoechoic central scar in 15-20%, displaces vessels around it, enlarged central artery and peripheral draining veins visible on DopplerCT: Ill-defined, transiently high attenuation in PV phase with gradual equilibration, central scar on delayed, ‘spoke-wheel’ pattern in 20-30%MR: Isointense on T1W and T2W, central scar hypointense on T1W and hyperintense (in 75%) on T2W; initial Gd avid enhancement with gradual equilibration (early enhancement of central scar); SPIOd (Kupffer specific) cause lesion enhancement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hepatocellular adenoma

A

Women on COCP and men on anabolic steroids, 20-40 y/o, usually 5-10 cm, subcapsular in right lobeContain mixture of hepatocytes, Kupffer cells and fat, but no portal tracts; usually contains haemorrhage and necrosisUS: Heterogeneous, solid, with hypoechoic rimCT: well defined, ±hyperdense if areas of haemorrhageMR: can’t be distinguished from HCC, predominantly hyperintense T1W and isointense T2WNM: Photopaenic on sulphur colloid, no uptake on Gallium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

HCC

A

Commonest visceral malignancy, peak 60-70 y/o;Solitary (30%), Multifocal (60-70%) and diffuse (5%) forms; invades PV in 50-60% and IVC in in siderotic noduleLarge HCC: Mosiac pattern (confluent nodules, small septae, best seen on T2W), tumour capsule (hypointense) in 60-80%, extracapsular extension with satellite nodules in 50-70%, tumour thrombus as high T1W and T1 GRE in PV, with arterial enhancementNM: photopaenic on sulphur colloid, avid uptake on Gallium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Fibrolamellar HCC

A

No RFs for HCC, 30-40 y/oSolitary lobulated lesion, central scar, pseudocapsule of hepatic tissue, central amorphous calcification in 30-40%Regional LNs 50-60%, rarely metastasises, no vascular invasionUS: Heterogeneous with hyperechoic central scarCT: Lobulated enhancing mass with non-enhancing central scarMR: Hypointense T1W, hyperintense T2W with heterogenous enhancement; scar hypointense on T1W and T2W and non-enhancing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Liver metastases

A

Usually colon, breast, lung or pancreas; solitary in 10%, both lobes in 75%US: variable, echogenic usually GIT or GU; no Doppler flow except with carcinoidExclusion criteria for metastatectomy - advanced primary, >4 metastases, extrahepatic metastases, <30% liver remaining post surgeryCalcified liver metastases: gastric, melanoma, RCC, colon, ovarianHypervascular metastases: thyroid, renal, carcinoid, melanoma, pancreatic islet cellHaemorrhagic metastases: Colon, thyroid, breast, choriocarcinoma, melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Budd Chiari Syndrome

A

Hepatic vein of IVC obstruction, 60-70% idiopathicCauses of thrombotic obstruction (5 P’s): Pregnancy, Pill, Polycythaemia Rubra Vera, abnormal Platelets, PNHNon-thrombotic obstruction: Right heart failure, constrictive pericarditis, right atrial tumour, IVC membraneUS: Hepatosplenomegaly, ascites, caudate lobe hypertrophy, ascites, prominent portosystemic anastomoses and azygos/hemiazygos systems, absent / reversed flow in hepatic veins, hepatic arterial resistance index >0.7CT: Heterogenous liver enhancement, caudate large and normally enhancing, poor opacification of hepatic veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hepatic veno-occlusive disease

A

Post radiation / chemotherapyMR: occlusion of centrilobular venules without major hepatic vein thrombosisUS: Bidirectional flow in portal veins without hepatic vein / IVC obstruction, GB wall thickening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Portal vein thrombosis

A

Causes: idiopathic (neonates), malignancy (in 30% of HCC, also cholangioCa, pancreatic Ca, liver metastases), hypercoaguable, trauma (iatrogenic - umbilical vein catheter), peritonitis, pancreatitis, ascending cholangitisUS: Echogenic material on PV, increased PV diameter, thickened lesser omentum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Peliosis hepatis

A

Rare benign dilatation of sinusoidal blood filled spaces in reticuloendothelial system (liver, spleen, marrow, lymph nodes, lungs)Causes: AIDS, TB, Anabolic steroids, CRF, tamoxifenUS: Multiple hyper-/hypoechoic areasCT: Enhancing, round lesions in organs; initially low attenuation then isoattenuating with time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Biliary anatomy

A

RPHD into LHD 20%RPHD, RAHD, LHD trifluence 10%75% cystic duct inserts into middle third of extrahepatic CHD, 10% distal CHDCBD / PD / Ampulla - 75% Y, 25% V, 5% UCHD measured at level of HA, normal <7 mmSecretin transiently distends pancreatic duct (maximal at 2 minutes post injection) prior to MRCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Choledochal cysts

A

Cystic dilatations of CBD; 30-40% present at <1 y/o.Clinical features: Intermittent obstructive jaundice, RUQ pain and RUQ mass (25% triad)Associations: Biliary, pancreatic anomalies and liver cysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Caroli’s disease

A

Segmental dilatation of intrahepatic bile ducts, autosomal recessive, causes biliary stasis with intrahepatic calculi then secondary pyogenic cholangitis, intrahepatic abscesses, increased risk cholangiocarcinomaAssociations: Medullary sponge kidney (80%), Infantile polycystic kidney disease’Central dot sign’ - specific, portal radicals surrounded by abnormally dilated / ectatic bile ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Chemotherapy cholangitis

A

Most commonly associated with floxuridine; strictures of CHD and bifurcation, sparing of distal CBD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cholelithiasis

A

Cholesterol (70-80%) but 70% mixed, 20% radiopaque, associated with cirrhosisPigment (30%) 2-5 mm, faceted, calcium bilirubinate, 50% radiopaqueWall-echo-shadow complex (double arc sign) when GB contracted over GS (but also seen with porcelain GB and emphysematous cholecystitis)Sludge (echogenic bile) - 100% fasting patients at 6 weeks (decreased CCK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Biliary Enteric fistulae

A

Most commonly biliary-duodenal (70%; can cause GS ileus)Causes: Chronic cholecystitis with GS erosion into GIT (90%), Penetration of posterior DU into CHD (5%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Bouveret syndrome

A

Obstruction of stomach or duodenum by GS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Mirizzi syndrome

A

Obstruction of CHD by stone in cystic duct; causes cholecystitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Complications of Acute cholecystitis

A

Usually GB wall > 3 mm, lumen distended > 4 cmMurphy’s sign 60% sensitive, 90% specific95% calculous, 5% acalculous (GB dysmotility with bacterial superinfection)Gangrenous cholecystitis (rupture), 20% mortality but neural death causes 60% Murphy’s negativeEmphysematous cholecystitis (ischaemia due to inflammation / vasculitis, rare; pneumobilia and air around GB on PFA; 40% diabetic)EmpyemaGS ileus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Xanthogranulomatous cholecystitis

A

Thickened GB wall with intramural nodules; can mimic adenoCaUsually 70-80 y/o femaleComplications (30%) - perforation, abscess, fistulae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Porcelain GB

A

Usually due to chronic cholecystitis (GB doesn’t react to CCK)Increased risk GB Carcinoma (15% lifetime risk)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

GB US in AIDS

A

Hepatosplenomegaly (30%), ascites (15%), lymphadenopathy (20%)GB wall thickening (7%; may be due to acalculous cholecystitis due to cryptosporidium, CMV)GS (6%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Cholangitis

A

Infection of obstructed bile ducts E coli > klebsiella > pseudomonas; 80-90% supparative60% due to GS or post surgical strictures, but can be due to ampullary tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

PSC

A

Chronic obliterative fibrosis of biliary tree, usually mostly intrahepatic, always involves CBDString of beads on cholangiogram, pruning of biliary tree10% risk cholangiocarcinoma; can also cause biliary cirrhosis.Associations: IBD, pancreatitis, Sjogrens, RPF, Peyronie’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Strawberry GB

A

Deposition of triglycerides and macrophages in GB wall, studded ‘strawberry’ appearance of wall (<1 mm echogenic lipid deposits, multiple 0.5 mm polyps)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

GB adenomyomatosis

A

Hyperplasia GB wall, enlarged Rokitansky-Aschoff sinuses, hypercontractile wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

GB adenomas

A

10% multiple, F>M, usually 5-20 mm, 60% associated with GSAssociated with Peutz Jeghers, FAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Cholangiocarcinoma

A

Usually at hilum or distal CBD (30-40%)Associations: GS (90%), PSC, Caroli’s disease, Biliary atresia, IBD (UC > Crohns), Porcelain GB (15% risk), familial polyposis, adult polycystic kidney disease, clonarchis (asians), toluene exposureIntrahepatic: Mass with satellite nodules, dilated biliary tree with hyperechoic mass; Klatskin tumour - at confluence of RHD and LHD (causing segmental dilatation of main ducts, PV obstruction and lobar atrophy)Extrahepatic: 10% present with cholangitis, pure intrahepatic biliary dilatation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

GB Adenocarcinoma spread

A

Direct invasion of liver (50%), liver metastases (5%)Direct invasion of duodenum (50%)Carcinomatosis (50%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Von Meyenburg Complex

A

Bile duct hamartoma, usually 1-5 mm, composed of disorganised bile ducts and fibrocollagenous stroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Pancreas Divisum

A

Lack of fusion of dorsal and ventral pancreatic ducts, 10% of population.Main pancreatic drainage is through the minor papilla (too small to handle secretions).25% of patients with recurrent idiopathic pancreatitis have pancreas divisum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Annular Pancreas

A

Abnormal migration of the ventral pancreas, surrounds and obstructs second portion of duodenumERCP: pancreatic duct encircles the duodenum.
Increased incidence of pancreatitis and peptic ulcer disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Complications of pancreatic trauma

A

Pancreatic fistula, 10%-20%Abscess, 10%-20%PancreatitisPseudocyst, 2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Types of Pancreatitis

A

Acute pancreatitis Mild acute pancreatitis (interstitial edema)Severe acute pancreatitis (necrosis, fluid collections)Groove pancreatitis: inflammation localized to groove between duodenum and pancreatic headChronic pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Pancreatic necrosis

A

Diffuse parenchymal (30% area) or focal (>3 cm) nonviable; CT 80-90% accuratePrognosis (necrosis/mortality): 30/8, 50/24, >90/50Infected necrosisRequires surgical debridement, can occur at any time, worse prognosis than pancreatic abscess.HamorrhageLate consequence, erosion into splenic or pancreaticoduodenal arteries or rupture of psuedoaneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Acute fluid collections pancreatitis

A

40% of pancreatitisNo fibrous capsule, usually within and around pancreatic periphery50% spontaneously resolve, remainder bocome pseudocysts or develop other issue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Pseudocyst

A

Encapsulated collection of pancreatic fluid due to microperforation of pancreatic duct (communication seen at ERCP in 50%), must persist at 6 weeks post onset.40% acute pancreatitis, 30% chronic pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Pseudocyst prognosis

A

Prognosis (<5 cm - monitor; otherwise percutaneous drainage; 10% risk superinfection)50% resolve spontaneously20% stable30% other complicationsDissection into adjacent organsHaemorrhage (vessel erosion, thrombosis, pseudoaneurysm)Peritonitis (rupture)Biliary obstructionInfection (abscess) - forms at 2-4 weeks, usually E coli, polymicrobial or candida if immunosuppressed; Percutaneously drained.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Emphysematous pancreatitis

A

Pancreatitis with superinfection, usually E Coli; high morbidity and mortality but usually resolves with conservative treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Chronic pancreatitis Types

A

Calcifying (alcohol, hyperparathyroisim/hypercalcaemia, hyperlipidaemia, hereditary pancreatitis, juvenile tropical pancreatitis)Obstructive (Trauma, Renal failure, CF, Sclerosing cholangitis, Ampullary tumour, ampullary stenosis)FeaturesFatty replacement, fibrosis, parenchymal calcifications (usually start in head), intraductal calculi.Irregular dilatation pancreatic duct (Grade 1-3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Complications of chronic pancreatitis

A

Malabsorption (50%)Pseudocyst (30%)Obstructed CBD (10%)Venous thrombosis (splenic, portal, mesenteric) (5%)Increased risk carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Autoimmune pancreatitis

A

Previously idiopathic pancreatitisHistologic diagnosis: dense lymphoplasmacytic infiltrate with scattered eosinophils. May be associated with autoimmune cholangitis. Treatment: steroids.Imaging: diffuse enlargement of pancreas, loss of normal surface indentations, tail retracted from splenic hilum, capsule-like rim enhancement around gland, peripancreatic adenopathy, no calcification, vascular encasement of CBD dilatation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Groove pancreatitis

A

Involves pancreatic groove (between pancreatic head, duodenum and CBD)Related to PUD, previous gastric resection, duodenal wall cysts, pancreatic heterotopiaBiliary strictures in 50%Imaging: Soft tissue in the pancreaticoduodenal groove with delayed enhancement; small cystic lesions along medial wall of duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Tropical Pancreatitis

A

Young, no C2H5, usually malnutrition, rapidly progressive, large intraductal calculi (>5 cm), x15-25 increased risk adenoCa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Hereditary Pancreatitis

A

AD, cationic trypsinogen gene mutation, 50-70x risk pancreatic adenocarcinomaSimilar to tropical pancreatitis on imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Heterotopic pancreatic tissue

A

Duodenum (30%)Stomach (25%) - usually submucosal along greater curveJejunum (15%)Rarely - Meckel’s, ileum, GB, fallopian tubes, umbilicus, oesophagus, spleen, mediastinum, omentum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Pancreatic Ductal Adenocarcinoma

A

95% pancreatic cancer; Couvosier’s sign (enlarged, nontender GB) in 25%; 8% 1 year survival65% head (5% curable), 35% body and tail (incurable)May be subtle hypodense on NECT, then hypodense on bolus contrast CT; calcifications rare; inverted 3 on barium meal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Pancreatic AdenoCa unresectability

A

Criteria for unresectabilitySMA encasedPortal vein or SMV largely encasedMetastases: Liver > LNs > pertioneal/serosal > lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

IPMN / IPMT

A

From epithelial lining pancreatic duct, secrete mucin, cluster of cysts 1-2 cm diameterPresents with abdominal pain ± pancreatitisCan be side branch (30%; usually in uncinate) or main duct or combined (70%)Associations - AdenoCa (25%), Hyperplasia (25%), Dysplasia (50%)Location: Head/uncinate (55%), Body/tail (10%), Multifocal/diffuse (35%)Increased risk of malignancy:Size > 3 cm or solitary and < 3cmSolid mass or mural noduleMain pancreatic duct > 10 mmIntraluminal calcificationsDiffuse or multifocalHx of DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Pancreatoblastoma

A

Usually 1-8 y/o, rareSometimes associated with Beckwith-WiedemannLarge, well-defined, multilobulated with enhancing septa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Solid pseudopapillary neoplasm

A

Aka Frantz’s tumour, usually female <50 y/oLarge epithelial well-demarcated mixed solid/cystic haemorrhagic mass

59
Q

Acinar cell carcinoma

A

Older males, usually larger and less desmoplastic than adenoCa, invades vessels, causes metastatic fat necrosis.

60
Q

Insulinoma

A

Most common islet cell tumour, usually 40-60 y/o, 90% sporadicSingle 90%, multiple 10%, diffuse hyperplasia / extrapancreatic 10%Malignant 10%90% < 2 cm but 70% hypervascularDiagnostic accuracy: intraoperative US > venous sampling > angiography > MRI > othersWhipple’s triad at presentation: symptoms of hypoglycaemia, hypoglycaemia, relief with glucose

61
Q

Gastrinoma

A

Second most common islet cell tumour, usually <20 y/o, 70% sporadic, presents with Zollinger-Ellison (diarrhoea, PUD)Usually benign (although 60% can have malignant transformation) but if MEN I then malignantUsually pancreatic head, but 30% ectopicGastrinoma triangle: Porta hepatis at apex, D2 and D3 as baseMean size = 3.5 cm

62
Q

Non-functioning islet cell tumour

A

Third most common islet cell tumour, associated with MEN I, peak age > 20 y/o80-100% malignant transformation (5 year survival 45%)Usually in pancreatic head, > 5 cm, hypervascular with hyperenhancing liver metastases, and 20% show calcification

63
Q

Glucagonoma

A

75% malignant, almost all symptomatic, associated with MEN IUsually 50-79 y/o, F>MUsually pancreatic body or tailPresents with Necrolytic Erythema Migrans (80%), Diarrhoea, DM, glossitis, VTE (25%)50% develop liver metastases

64
Q

VIPoma

A

67% female, 60% malignant, 59% liver metastases at presentationUsually pancreatic body/tail but extrapancreatic sites - RP, mediastinum in children (usually from neurogenic tumour)Presents with Verner-Morrison’s syndrome: watery diarrhoea, hypokalaemia, hypochlorhydriaOften causes GB dilatation due to VIP causing smooth muscle paralysis

65
Q

Somatostatinoma

A

90% malignant, usually pancreatic headPeak 50 y/o, presents with DM, steathorrhoea (suppresses insulin, TSH, GH secretion)

66
Q

Pancreatic metastases

A

RCC (usually hypervascular), lung, breast, GIST, melanoma, carcinoid, adrenal, thyroid, angiosarcomaUsually head of pancreas

67
Q

MEN

A

I (Wermer’s): PTH, pancreas (islet cell), anterior pituitary ± mutiple limpoas and angiofibromasIIA (Sipple’s): Commonest MEN, usually RET oncogene positive; causes medullary C cell thyroid carcinoma, phaeochromocytomas (70% bilateral), PTH gland hyperplasia; associated with carcinnoid and Cushing’s syndromesIIB: 5% of MEN II, marfanoid features, mucosal neuromas; medullary thyroid carcinoma, phaeochromocytomas, oral and intestinal mucosal neuromas, intussusception due to small bowel neuromas

68
Q

Carney’s Complex

A

Rare form of MENPresents with primary pigmented adrenocortical disease, pituitary adenomas, sertoli cell tumours, thyroid nodules, cardiac myxomas, schwannomas

69
Q

Whipple’s Surgery and complications

A

Resection of pancreatic head, duodenum and gastric antrum, usually with cholecystectomy;Usually jejunal loop used to anastomose resected portionsComplicationsDelayed gastric emptying (11-29%): NG tube required > 10 daysPancreatic fistula: surgical drain output of amylase rich fluid at >5 mL/day at >7-10 days (10-15% require percutaneous drainage, 5% require further surgery)Infection, abscess, haemorrhage, pancreatitis

70
Q

Pancreatic transplant

A

Duodenal interposition between pancreas and bladder, duodenocystostomyComplications:Rejection (35%)Pancreatitis (35%)Peripancreatic abscess (35%)Peripancreatic haemorrhage (35%)Vascular thrombosis (20%)

71
Q

Oesophageal atresia / Types of tracheo-oesophageal fistula

A

A: Atresia without fistula (10%)B: Atresia with proximal TOF (<1%)Polyhydramnios: 33% of fetuses with atresia and distal TOF, 100% of atresia without fistulaGasless stomach: Type A and BRight sided aortic arch in 5% of TOF patients

72
Q

Iatrogenic TOF

A

Usually at carina, can be caused by ET cuff; also by blunt trauma

73
Q

Malignant TOF

A

Usually oesophageal malignancy; less likely lung Ca, SCC larynx50% trachea, 40% bronchi

74
Q

Oesophageal Cancer

A

4-10% GI malignacy, M/F = 4/1;SCC 50-70%, Adenocarcinoma 30-50%20/30-40/30-40 = upper/middle/lower thirdsT: 3=adventitia, 4=adjacent structuresEUS best for local staging

75
Q

Oesophageal Cancer Unresectability Criteria

A

Pericardial effusionIntraluminal airway massTumour between arch and trachea or left main bronchus and descending aortaPleural thickening or pleural effusion adjacent to tumourMediastinal or coeliac axis nodes

76
Q

Oesophageal perforation

A

55 % iatrogenicif upper oesophageal, usually at cricopharyngeus, causing widening of prevertebral fascia, air/fluid and a right pleural effusion

77
Q

Boerhaave’s syndrome

A

Failure of cricopharyngeus to relax with pressure rise and ruptureUsually tear at left posterolateral wall of lower oesophagus 2-3 cm proximal to GOJSecond commonest rupture at upper thoracic area or subdiaphragmatic30% mortality but better surgery at 24, 90% at >48 hoursCXR 90% abnormal, usually a unilateral effusion

78
Q

V sign of Naclerio

A

Only in 20% Boerhaave’s, but specific - air in space between heart and vertebral column, thus left paraspinal hyperlucency

79
Q

Oesophageal ring

A

3-5 mm extension of 3 layers (mucosa, submucosa, muscle)A: 1.5 cm proximal to z lineB (Scatzki): technically web as only mucosa and submucosa, at z line, upper limit of HHC: Rare anatomical variant, represents indentation of diaphragmatic crura

80
Q

Oesophageal strictures

A

Peptic (70-80%), originate from z line, 1 to 4 cm long, whites increased risk x10, M/F = 2.5/1Smooth: Inflammatory (peptic, scleroderma, corrosive), Neoplastic (Ca, leiomyoma), Achalasia, Skin (Epidermolysis Bullosa, pemphigus)Irregular: Neoplastic (Ca, leiomyosarcoma, lymphoma), Inflammatory (acid reflux, Crohn’s), Iatrogenic (Radiotx, fundoplication)

81
Q

Oesophageal varices

A

Due to increase of portal pressure above normal (i.e. >10 mm Hg)Gastrooesophageal varices: Left gastric (coronary) vein and short gastric veins (via splenic hilum)Paraoesophageal varices: outside oesophageal wall

82
Q

GORD and HH’s

A

Grades: I - erythema, II - linear non-confluent erosions, III - circular confluent erosions, IV - stricture, BOSliding HH - >1.5 cm difference between GOJ and diaphragmParaoesophageal HH - fundus herniates and GOJ remains below diaphragmType 3 HH - combined sliding and paraoesophagealType 4 HH - All / part of stomach with some organoaxial rotation

83
Q

Barrett’s Oesophagus

A

Squamous to columnar metaplasia, 0.5%/year progression to AdenoCa (not reduced by fundoplication), thus oesophagectomy indicated if dysplasia confirmed by second pathologistRF: GORD, HH (75-90%), reduced LOS pressureReticular pattern on Ba swallow, strictures occurs at squamocolumnar junction (usually short, tight and eccentric)

84
Q

Candida Oesophagitis

A

Usually oral thrush but absent in 25%Tends to be in upper oesophagus and longitudinally orientated plaques, progresses to ‘shaggy’ confluent plaques and pseudomembranes in AIDS patients, can dissect with contrast - ‘double barrel’ oesophagus

85
Q

Tuberculous oesophagitis

A

Erosion of enlarged mediastinal nodes into oesophagus, causing shallow ulcers and heaped up lesions with extrinsic oesophageal compression

86
Q

CMV Oesophagitis

A

Severe odynophagia and dysphagia, evidence of dissemination≥1 giant superficial diamond/ovoid/serpiginous erosion in mid/distal oesphagus, may be up to 5-10 cmCan have satellite ulcers and halo of oedematous tissue

87
Q

HSV Oesophagitis

A

Second commonest, usually rounded 1-3 mm vesicles in mid-distal oesophagus with halo of oedemaCan be indistiguishable from candida if advanced (plaques, cobblestone, shaggy)VZV can be similar but has an associated skin rash (shingles)

88
Q

HIV Oesophagitis

A

Acute onset odynophagia, maculopapular rashGiants flat ulcers ≥1 cm with satellite ulcers and rim of oedema (very similar to CMV)Can result in perforation, fistulae, superinfection

89
Q

Oesophageal Leiomyoma

A

Commonest benign oesophageal tumour, usually distal oesophagus (smooth muscle)Can be associated with HPOA, can show calcification

90
Q

Zenker’s diverticulum

A

Between inferior constrictor and cricopharyngeus, usually at posterior left oesophagus

91
Q

Alport’s

A

Multiple oesophageal leiomyomas, sensorineural deafness, renal impairment

92
Q

Grades of Candida oesophagitis

A

Grades - 1: Few raised plaques ≤2 mm, no ulceration2: Multiple raised white plaques >2 mm, no ulceration3: Confluent linear nodular elevated plaques with ulceration4: Grade 3 with stricturing, thus narrowed oesophageal lumen

93
Q

Lateral pharyngeal pouch and diverticulum

A

Occurs in glass blowers and musicians through thyrohyoid membrane at anterolateral upper hypopharynx

94
Q

Lateral cervical oesophageal pouch and diverticulum

A

Through Killian Jamieson space below cricopharyngeus, usually asymptomatic

95
Q

Tertiary oesophageal contractions

A

Non-propulsive, usually due to muscle atrophy, in 25% >60 y/oCauses: Reflux, presbyoesophagus, neuropathy, DM, alcohol, malignant infiltration or gastric cardia obstruction, early achalasia

96
Q

VACTERL

A

3 or more of following anomaliesVertebral: hemivertebrae, scoliosis, rib deformitiesAnorectal: Imperforate anus, cloacal deformityCardiovascular: VSD, tetralogy of Fallot, PDA, ASD, AV canal defects, aortic coarctation, right sided aortic arch, single umbilical arteryTracheo-oesophageal: Oesophageal atresiaRenal: renal agenesis (Potter’s syndrome, bilateral agenesis), horseshoe kidney, polycystic kidneys, urethral atresiaLimb: Radial dysplasia/absence, syndactyly, polydactyly, tibial deformities

97
Q

Phlegmonous Gastritis

A

Rare, due to strep, staph, proteus, clostridium, E ColiUsually debilitated patients; often recent alcohol binge, URTI and AIDS

98
Q

Emphysematous Gastritis

A

Widespread phlegmonous gastritis, with mucosal disruption and gas in stomach wallFoul smelling bloody vomit with necrotic cast of stomach (pathognomic)

99
Q

Corrosive gastritis

A

Acid: Severe gastric damage, oesophagus unharmedAlkali: Pylorus and antrum usually involved

100
Q

Gastric cancer

A

3rd commonest GI malignancy, 95% adenoCa, 5 year survival 5-18%Usually distal third or cardia; 60% lesser curve, 10% greater curve, 30% GOJT Stage: 3 penetrates serosa, 4a invades contiguous tissues, 4b adjacent organs / diaphragm / abdominal wallRFs: Smoking, nitrates, H Pylori, atrophic gastritis, pernicious anaemia, Menetriers, gastrojejunostomy/partial gastrectomyMetastases: Liver (25%), peritoneal seeding to rectum (Blumer’s shelf), ovaries (Krukenberg), left suprclavicular (Virchow’s node)

101
Q

Peptic Ulcer

A

Risk of malignant transformation 2% in initial 3 yearsGastric: Pain after eating, if benign usually on lesser curve, project beyond stomach contour, mucosal folds radiating to ulcer marginMalignant ulcer - irregular, heaped up margins, protrude into lumen of stomachDuodenal: Pain relieved by food, occurs hours after meals and at night, 95% in D1, usually <1 cm

102
Q

Gastric volvulus

A

Subdiaphragmatic (30%) or Supradiaphragmatic (60%; associated with paraoesophageal rolling HH)Axis: organoaxial (60%; axis of rotation parallel to lesser curve; 30% necrosis) or mesentroaxial (30%; axis perpendicular to lesser and greater curves; usually intermittent and vascular compromise rareSevere pain and retching without vomiting, can’t pass NG tube

103
Q

Pyloric Stenosis

A

Inherited as dominant polygenic trait, higher incidence in first born malesCauses hypokalaemic, hypochloraemic metabolic alkalosisUsually presents at 2-8/52 with non-billous projectile vomiting and palpable olive shaped massUS: Target sign (hypoechoic ring of hypertrophied pylorus around echogenic central mucosa), elongated pylorus (≥17 mm), increased pyloric muscle wall thickness (≥3 mm), pyloric transverse diameter ≥13 mm

104
Q

GIST

A

Commonest mesenchymal GI neoplasm, 50-70% in stomach, then SI, mesentery, omentumSubmucosal and endophyticAssociations: NF1, Carney’s triad (GISTs, pulmonary chondromas, extra-adrenal paragangliomas)CT: Rim or homogenous enhancement, ±calcification and necrosis

105
Q

Causes of Linitis Plastica

A

Neoplastic: Gastric carcinoma, lymphoma, metastases, local pancreatic cancer invasionInflammatory: Corrosives, radiotherapy, granulomas, eosinophliic enteritis

106
Q

Causes of gastric target lesions

A

Submucosal metastases (melanoma, lymphoma, carcinoma, carcinoid)LeiomyomaEctopic pancreatic tissue (pancreatic rest)Neurofibroma

107
Q

Haemoperitoneum

A

Serum: 0-20 HUFresh unclotted: 30-45 HUClotted: 50-100 HUActive Bleed: >180 HUSentinel clot - highest attenuation clot, site of injury

108
Q

CT Signs of hypovolaemia

A

Collapsed IVC (20 HU above liver, with peripancreatic oedema, mesenteric and RP fluid collectionsIntense adrenal enhancement (>IVC)Mucosal enhancement of GB and bowel (shock bowel - >psoas muscle, >3 mm mural thickening, fluid filled/dilated >2.5 cm)

109
Q

Sites of blunt bowel trauma

A

In order of decreasing frquencyJejunum distal to ligament of TreitzDuodenumAscending colon at ICVDescending colon

110
Q

Bowel injury signs on CT

A

Extraluminal contrast 100% Sp, low Sn; extraluminal air 40-50% Sn, usually duodenal injuryBowel wall thickening 75% transmural injuries, high Sn, may also be seen in isolated mesenteric lacerationsMesenteric stranding particularly on mesenteric borderHaemoperitoneum and haematoma in mesenteryFree fluid on three contiguous sections suggests significant bowel or mesenteric injury5% hepatic and splenic lacerations associated with major bowel injuryFocal discontinuity of bowel wall

111
Q

Malrotation

A

Arrest of gut rotation and fixation, can cause midgut volvulus and duodenal obstructionCT: SMV on left of SMA in 80%

112
Q

Spigelian hernia

A

Ventrolateral hernia through defect in aponeurosis of transverse and rectus muscles

113
Q

Lumbar hernias

A

GrynfeltPetit’s lumbar triangle

114
Q

Obturator hernia

A

Between pectineus and external obturator

115
Q

Inguinal hernia

A

Direct: via defect in Hesselbach’s triangle, medial to inferior epigastric vesselsIndirect: via inguinal canal, lateral to inferior epigastric vessels

116
Q

Richter’s hernia

A

Entrapment of anti-mesenteric border of bowel in hernial orifice, usually older women in femoral hernia

117
Q

Internal hernias

A

Via developmental or surgical defect in peritoneumParaduodenal - congenital defect in descending mesocolonLesser sac - via foramen of Winslow in retrogastric locationHiatus hernia - 99% sliding (GOJ in chest), 1% paraoesophageal (GOJ below diaphragm, upper stomach in chest)

118
Q

Duodenal diverticulum

A

Commonest at D1, can cause perforation, biliary or bowel obstruction, bleeding, diverticulitisPrimary: Mucosal prolapse through muscularis propriaSecondary: All layers of duodenal wall, due to duodenal inflammation

119
Q

Cobblestone duodenal cap causes

A

Big cobblestones: Hypertrophy of Brunners glands, Crohn’s, Varices, Carcinoma, lymphomaSmall cobblestones: Food residue, duodenitis, nodular lymphoid hyperplasia, heterotopic gastric mucosa

120
Q

Decreased or absent duodenal folds

A

AmyloidCrohn’sCFSclerodermaStrongyloidiasis

121
Q

Thickened duodenal folds

A

Inflammation: Crohn’s, duodenitis/pancreatitis, Zollinger EllisonInfiltrative: Neoplastic (Metastases, lymphoma), eosinophilic enteritis, amyloid, mastocytosis, Whipple’sVascular: Intramural haematoma, ischaemiaOedema: Hypoproteinaemia, venous/lymphatic obstruction, angioneurotic oedemaInfective: Worms, giardiasis

122
Q

Causes of duodenal dilatation

A

Mechanical obstruction (bands, atresia, annular pancreas, SMA syndrome)Paralytic ileusScleroderma

123
Q

Intestinal lymphoma

A

Commonest SI malignancy, commonest cause of intussusception in children >6 y/oRFs: Coeliac, AIDS, SLE, Crohn’s, chemotherapyLarge cavitating ulcerating / nodular mass with aneurysmal SI dilatationPoor prognosis unless low grade, MALToma = low grade B cellCT: Polypoidal / nodular (47%), diffuse infiltrative (11%; reduced peristalsis), ulcerative (42%; can perforate)Staging: I - Bowel wall, II - local nodes, III - widespread nodes, IV - disseminated (e.g. liver, marrow)SI locations (arise from Peyer’s patches): 51% ileum, 47 % jejunum, 2% duodenumCan cause desmoplastic responeseEndoexoenteric lymphoma: large mass, small intramural component, can cause fistulation

124
Q

Gastric lymphoma

A

Presentation of 2.5% of lymphomas, commonest site of extranodal spreadCan have nodular mass (25%), diffuse involvement without ulcers (50%), ulceration (8%)

125
Q

Colonic lymphoma

A

85% caecum

126
Q

Carcinoid

A

Commonest SI primary; 2% 2 cm metastasise (usually ileal)33% small bowel (81% ileum, 7% jejunum, 2% duodenum, 10% gastric), 45% appendix (rarely metastasises)33% second primarySecretes 5-HIAA, ACTH, histamine, serotonninGastric: Usually solitary fundal lesion, 50-70% metastases at presentationDuodenal: Intraluminal polypoid (50%) or intramural (40%), arterial enhancement with delayed washout (unlike ampullary tumours)Jejunal/ileal: Can cause invasion, fibrosis, ‘hairpin turn’ in bowelMetastases: Liver, LNs, lung, bone

127
Q

Coeliac Disease

A

Bimodal: 1-3 y/o and 30-50 y/o, F/M = 2/1Primarily involves SI mucosa with atrophic villi with elongated crypts, typically worse in jejunum than ileumDiagnosis: Reversal of jejunal/ileal fold pattern (due to ileal hypertrophy; jejunal atrophy (≤3 folds per 2.5 cm in first jejunal loop, with increase in ileal folds) + 3 of: fold thickening, SI dilatation, flocculation (hypersecretion, 20-30%)Can cause gastric metaplasia in duodenum with mucosal nodules (bubbly bulb)Extraintestinal features: anaemia, osteopaenia, dermatitis herpetiformis, amenorrhoeaComplications: Ulcerative jejunitis (usually fatal), Intussusception, cavitating lymph node syndrome, hyposlenism and splenic atrophy (30-50%), small bowel lymphoma, adenoCa of SI/rectum/stomach, Oesophageal SCCAssociations (10%): Autoimmune thryoiditis, Sjogren’s

128
Q

Whipple’s Disease

A

Gram positive tropheryma whippelii disordered host response, usually immunocompromised patients, M/F = 8/1Muscle wasting, arthralgia, fever, diarrhoea, pericarditisPositive periodic acid Schiff macrophagesFatal in <1 year if untreated by antibioticsMinimal bowel dilatation, thickened jejunal and ileal folds, bulky hypodense LNs

129
Q

Radiation enteritis

A

Required dose: 45-60 Gy SI, 55-80 Gy colonAcute (within 6-24 months) severity function of dose, field and type; chronic of cumulative doseRFs: HTN, DM, PID, combination chemo-radiotherapy, previous abdominal surgerySubacute phase (2-12 months) due to obliterative endarteritis of small vesselsChronic (>1 year) fibrosis, adhesions, fistula, increased mesnteric attenuation

130
Q

Radiation injury of stomach

A

Usually 45-60 Gy over 5 weeksAcute phase - 2-8 weeks post Rx; chronic 4 weeks to 7 months post RxTypes: 1. Prepyloric or Pyloric ulceration - Usually acute, indistiguishable from benign ulcers2. Antral narrowing - chronic injury, no ulceration, may mimic gastric cancer

131
Q

Radiation injury colon and rectum

A

Increase presacral space >1 cm, thickening/effacement valves of Houston, halo effect on CT (increased attenuation prerectal fat and fibrous tissue)

132
Q

GvHD

A

Loss of haustrations, tubular SI, persistent coating of bowel mucosa by barium, reduced transit

133
Q

Appendicitis

A

Causes: faecolith obstruction (33%), lymphoid hyperplasia, foreign body, parasites, tumourUS: Wall thickness >2mm, graded compression 85% Sn, 92% SpCT: 87-100% Sn, 89-98% Sp, >7 mm diameter

134
Q

Meckel’s Diverticulum

A

Persisting omphalomesenteric duct on antimesenteric ileal border; 50% contain ectopic mucosa (gastric, pancreatic, coloonic)Rule of two: 2% population, 2 inches long, 2 feet from ICV, symptomatic before 2 y/o (but 20-40% asymptomatic)Compilcations: Bleeding, intussusception, obstruction, malignancyTc99m: 85% Sn, 95% Sp (but drops with age as less gastric mucosa in Meckel’s with age)Angiogram: Identification of vitelline artery is pathognomic

135
Q

Chronic mesenteric ischaemia

A

> 95% due to diffuse atherosclerotic disease, causes mesenteric anginaTreatment: Coeliac/SMA endartectomy, bypass, mesenteric artery reimplantation (not recommended)

136
Q

Epiploic appendagitis

A

Abrupt onset pain in RLQ (50%), palpable mass 10-30%CT: pericolic oval 1-4 cm mass; hyperechoic on US with hypoechoic marginPrimary: due to torsion or venous thromboisSecondary: inflammation of adjacent organ

137
Q

Infective TI lesions

A

TB, yersinia, Actinomycosis, histoplasmosis

138
Q

Ischaemic Colitis

A

Non-occlusive but blood flow s point - anastomotic plexus between IMA and hypgastric supply at rectosigmoid junctionCT: Segmental thickening, portal/mesenteric gas

139
Q

Pseudomembranous colitis

A

C Difficile - GPB, anaerobic and spore forming; Toxins A (enterotoxin) and B (cytotoxin), 25% mortality in elderlyUsually due to cephalosporins, ampoicillin, amoxicillin, clindamicinPancolitis (50%), right sided colitis (27%), isolated rectosigmoid (12%), but rectosigmoid spared in 67%Stool cytotoxin 94% Sn, 99% Sp; 2-10 m yellow pseudomembranes on endoscopyComplications: fulminant colitis (3%), toxic megacolon, colonic perforation, peritonitisCT: Mural thickening, bowel dilatation, paucity of pericolonic inflammation

140
Q

Diverticular disease

A

Mucosal herniations through intestinal layers/smooth musclle via vasa recta apertures; 70-80% >80 y/o10-25% risk of diverticulitisComplications: Abscess, fistula (14%), perforation, sepsis, bleeding (more likely in diverticulosis)

141
Q

Colonic polyps

A

Colonic mucosal outgrowths, 1.5 cm, have 10% risk of containing invasive cancerCT colonography detects 80% large polyps, colonoscopy 80-90% sensitive

142
Q

Colorectal carcinoma

A

RFs: Family history, polyps (30-40% villous, 5% tubular), IBD, prominent lymphoid follicular pattern, obesity, asbestos, Lynch syndromeLocation: Rectum (30%), sigmoid (30%), descending (10%), transverse (10%), ascending (10%), caecum (10%)Metastases: Liver (75%), adrenal (10%), lung (5-50%), ovary (5%), bone (5%), brain (5%)Dukes staging (5 yr survival): A (85%) - mucosa, B (70%) - muscularis propria, C (33%) - lymph nodes, D (5%) - metastases33% recurrence, half within one year, 60% locally (risk reduced by radiotx)

143
Q

Crohn’s disease

A

RFs: Family history, smoking, OCPComplications: sinus tracts (15%), bowel obstruction (20%), fistulae (50%), malignant transformation (usually adenoCa)Ulceration usually along mesenteric bordersCobblestoning causes reticular pattern’String sign’ due to stricturingMesenteric stranding does not necessarily correlate with disease activity

144
Q

Ulcerative colitis

A

Crypt abscess formation, inflammation usually progresses proximally from rectum, can cause backwash ileitis (incompetent ICV), benign strictures in 10% with chronic diseaseCRC risk increases by 0.5-1% per year after 10 years;Toxic megacolon (2%) - dilatation >9 cm in caecum, 10 cm in transverse colon carries high risk perforationBa enema (while quiescent): rose thorn ulcers, collar button ulcers (undermining of edges), CT: Rectal narrowing causes increased presacral space, target sign (alternating high and low attenuation colonic wall due to oedema), submucosal fat deposition UC>Crohn’sUS: Can differentiate UC from Crohn’s in skilled hands because transmural inflammation

Z3. GI FRCR 2A Primer (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions