GIT 2 Flashcards

1
Q

What is this condition?

What does it predispose to?

A

Jejunal (+/- ileal) diverticuli

outpouchings may predispose to:

  • bacterial overgrowth
  • Vit B12 deficiency
  • Megoblastic anemia

Jejunoileal diverticula

Dr Michael P Hartung◉ and Dr Bruno Di Muzio◉◈ et al.

Jejunoileal diverticula, also referred to as jejunal diverticula or diverticulosis as most of the diverticula are located in the jejunum, are outpouchings from the jejunal and ileal wall on their mesenteric border that represent mucosal herniation through sites of wall weakening 1.

Jejunoileal diverticulitis is much rarer than colonic diverticulitis.

See also

Please refer to the articles on duodenal diverticula and on Meckel diverticulum for a discussion of other small intestine diverticular disease.

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2
Q

What is blind loop syndrome?

A
  • syndrome develops after bypassing SB by an entero- anastomosis with subsequent stagnation of bowel contents.
  • Malabsorption in large diverticulae may cause similar dynamics.
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3
Q

What is malabsorpation re small bowel and what are the imaging features?

A
  • Abnormal absorption of fat, water, protein and carbs from the SB
  • Imaging features:
    • dilation of bowel
    • diluted barium (mixes with watery bowel content)
    • Flocculated barium
      • barium aggregates into partcles
    • Slow transit
    • segmentation of barium
      • lack of continuous column, rarely occurs with new agents
    • Moulage pattern
      • featureless barium collection
    • Hidebound pattern:
      • valvulae thinner, closer together
      • wrinkled look

Moulage sign (bowel)

Dr Jeremy Jones◉ et al.

The moulage sign is related to sprue, in particular coeliac disease. It occurs where there is a dilated jejunal loop with complete loss of jejunal folds 1. It is said to appear like a tube into which wax has been poured.

History and etymology

Moulage (French: casting/moulding) is the art of applying mock injuries to aid in the education of medical emergency teams. It was used as early as the renaissance when wax figures were used.

https://www.researchgate.net/figure/Findings-of-malabsorption-at-barium-examination-a-Image-shows-duodenitis-with_fig1_51501338

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4
Q

Three types of Sprue

A
  • Tropical sprie
    • Unknown cause, responds to Abx
  • Nontropical
    • adules
    • intolerance to gluten in when and other grains
    • HLA RD3, IgQA, IgM antibodies
  • Celiac disease (kids)

Sprue

Dr Daniel J Bell◉ and Dr Jeremy Jones◉ et al.

Sprue is the collective term for the malabsorptive gastrointestinal enteropathies although it may be used to refer directly to tropical sprue. It is composed of two entities:

tropical sprue

non-tropical sprue/coeliac disease

In each, the radiologic features are not sensitive enough to confirm an absolute diagnosis. However, they do help to characterise the disease process. The gold standard investigation is upper GI endoscopy with duodenal biopsy.

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5
Q

Imaging features of Sprue:

A
  • dilatation of small bowel
  • nodular changes in duodenum (bubbly appearance)
  • Reversal of jejunal and ileal fold patterns
  • Segmentation
  • hypersecreation and mucosal atrophy cause the Moulage sign (rare)
  • Transient intussusception pattern (coiled spring) is typical
  • Increaased secreations: flocculation with older barium suspensions
  • Increased incidence of malignancy, aggressive lymphoma, carcinoma
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6
Q

Disorders a/w Sprue (5)

A
  1. Dermatitis herpetiformis
  2. slective IgA deficiency
  3. Hyposplenism
  4. Adenopathy
  5. Cavitary mesenteric LN syndrome
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7
Q

Complications of Sprue

A
  • Ulcerative Jejunoileitis:
    • several segments of bowel wall thickening with irregularity and ulceration strictures may follow
    • Enteropathy: associated T-cell lymphoma
    • Increased incidence of Cancers of the oesophagus, pharynx, Duodenum and rectum
    • Sprue, SBO, Sclerderm (SOS): dilated, prolonged motility, normal folds.
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8
Q

What is mastocytosis?

Clinical findings

Imaging findings

A
  • Systemic mast cell proliferation in Reticuloendothelial system (SB liver spleen , LNs bone marrow and skin, with histamine release
  • Clinical findings:
    • diarrhea
    • steatorrhea
    • histamine effects
      • flushing
      • tachycardia
      • pruritis
      • PUD
  • Imaging:
    • SB:
      • irregular fold thickening
      • diffuse small nodules
    • Other:
      • Sclerotic bone lesions
      • Hepatosplenomegaly
      • PUD
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9
Q

What is Amyloidosis?

How to Dx?

A
  • Heterogenous group of disorders
  • abnormal extracellular deposition of insoluble fibrillar protein material
  • Dx
    • bx of affected organs
    • birefringence
    • staining with congo red
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10
Q

What are the major clinical amyloidosis syndromes?

A
  • Systemic Amyloidosis
    • immunocyte dyscrasia
      • myeloma
      • Monoclonal gammopathy
    • chronic/active disease
    • hereditary syndromes
      • neuropathy form
      • nephrophatic form
      • cardiomyopathic form
    • Chronic Hemodyalisis
    • Senile Form
  • Localised Amyloidosis
    • cerebral amyloid angiopathy
      • Alzheimer disease
      • senile dementia
    • Cutaneous form
    • Ocular form
    • others
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11
Q

What chronic/active diseases are a/w Systemc Amyloidosis?

A
  • Infections
    • TB
    • Chronic OM
    • Decubitus Ulcers
    • Bronchiectasis
    • Chronic Pyelo
  • Chronic inflammatory disease
    • RhArthritis (5-25% of cases)
    • AnkSpond
    • Crohns disease
    • Reiter Syndrome
    • Psoriasis
  • Neoplasms
    • Hodgkin Disease (4% of cases)
    • RCC (3% of cases).
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12
Q

Imaging featuers of Amyloidosis

Renal

GIT

Heart

CNS

A
  • Renal
    • neprotic syndrome
    • Renal insufficiency
    • Renal tubular acidosis
    • Renal vein thrombsosis
  • GIT
    • diffuse thickening of SB folds
    • Jejunisation of ileum
    • SB dialtion
    • multiple nodular filling defects >2mm
    • Hepatosplenomegaly
    • macroglossia
    • colonic pseudodiverticulosis
  • hearth
    • cardiomyopathy (restrictive)
    • rhythm abnormalities
  • CNS
    • dementia
    • Carpal Tunnel sundrome
    • Peripheral neuropathy.

Radiographics article:

https://pubs.rsna.org/doi/10.1148/rg.2021210006

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13
Q

What is Intestinal Lymphangiectasia?

what are the two forms?

A
  • spectrum of lymphatic abnormality
  • dilated lymphatics in Lamina propria of SB
  • Clinically reslts in protein losing enteropathy
  • The congenital form (infantile)
    • generalised lymphedema
    • chylous pleural effusions
    • diarrhea, steatorrhea
    • lymphocytopenia
  • Aquired/Adult form is the result of
    • obstruction of the thoracic duct
      • radiation
      • tumours
      • retroperitoneal fibrosis
    • SB lymphoma
    • Pancreatitis.

https://www.semanticscholar.org/paper/MRI-in-Primary-Intestinal-Lymphangiectasia%3A-A-Tool-Varma-Jana/c7a775f543215caae95dd0270f1cada7a5ddc146/figure/1

Figure 2: MR images of a 11 month female child with intestinal lymphangiectaisa. Coronal HASTE (a) and axial T2W spin echo fat saturated (b) images show ascites and diffuse thickening of the mid and distal jejunal and ileal loops. There are multiple tubular and tortuous hyperintense channels in the jejunum (arrow); note the normal thickness of the proximal jejunal walls (block arrow)

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14
Q

Imaging features of Intestinal lymphangiectasia

A
  • Diffuse nodular thickening of folds in jejunum and ileum caused by dilated lymphatics and hyoalbuminemic edema
  • Mesenteric adenopathy on CT.
  • Dilution of contrast material as a result of hypersecretion.
  • Lymphographic studies
    • hypoplastic lymphatics of lower extremity
    • tortuous thoracic duct
    • hypoplastic LNs
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15
Q

GI Lymphoma

A
  • Distinct subgroup of lymphoma that primariliy arises in lymphoid tissue of the bowel rather than in LNs
    *
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16
Q

WHAT does MALT stand for?

A
  • Type of GI lymphoma
  • Gastric lymphoma arising from Mucosal associated lymphoid tissue (MALT)
  • Muscosal associated lymphoid tissue
    • usually low grade malignancy
    • represents 20% of malignant SB tunmours.
    • usual age is in the 5th to 6th decades
  • Imaging features
    • Mass, nodule, fold thickening (focal or diffuse)
    • Confined to the GIT in 50%
    • Adenopathy in 30%
    • Extra abdominal findings 30%
  • Large ulcerated mass presenting as endoenteric or exoenteric tumour
    • DDx
      • GI stromal Tumour
      • metastatic Melanoma
      • Jejunal diverticulitis with abscess
      • ectopic pancreas
  • aneurysmal dilation
    • localized dilated tick walled, noncontractile lumen bc of mural tumor
    • Auerbach plexus neuropathy
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17
Q

DDx for a Large ulcerated mass presenting as endoenteric or exoenteric tumour

A

Large ulcerated mass presenting as endoenteric or exoenteric tumourDDx

  • GI stromal Tumour
  • metastatic Melanoma
  • Jejunal diverticulitis with abscess
  • ectopic pancreas
  • MALT
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18
Q

Which type of GI lymphoma do immunosupressed patients get?

A
  • Immunosupressed/HIV patients usually get aggressive NHL with rapid spread, poor response to chemo and short survivial
  • widespread extraintestinal involvement 80%
  • Imaging features
    • nodules
    • fold thickening
    • mass
    • splenomegaly 30%
    • Adenopathy 30%
    • Ascites 20%
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19
Q

What is Graft Vs Host reaction (GVH)

A
  • Donor lymphocytes react against organs (GIT, SKin, liver) of the recipient after Bone marrow transplant
  • Pathology
    • granular necrosis of crypt epithelium

Imaging features:

  • Ribbon Bowel
  • luminal narrowing is due to edema of the bowel wall
  • flattening of mucosal folds (edema)
  • prolonged coating of barium for days.
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20
Q

What sign is this and which disease is it seen in?

what GIT and non-GIT signs of this disease are possible?

A
  • AKA Progressive systemic sclerosis
  • systemic disease that involves primarily skin, joins and the GIT
  • Esophagus>SB>colon>stomach
  • Age 30-50 years
  • Female > Male

Imaging features

  • SB
    • dilation of bowel loops with hypomotility KEY FEATURE
    • Mucosal folds are tight and closer together (fibrosis) HIDEBOUND APPEARANCE
    • Pseudosacculations along antimesenteric border may involve both small and large bwoel.
    • Segmentation, fragmentation and hypersecretion are ABSENT.
  • Other
    • dilated dysmotile oesophagus, oesophagitis, incompetent LES, Reflux stricture
    • dilated duodenum and colon (pseudoobstruction)
    • Pneumatosis cystoids coli (steroid therapy)
    • Pulmonary intersitial fibrosis
    • Acroosteolysis
    • Soft tissue calfdication.

Hide-bound sign (bowel)

Dr Evyn Arnfield and Dr Andrew Dixon◉ et al.

The hide-bound bowel sign refers to an appearance on a barium study of the small bowel in patients with scleroderma. The sign describes the narrow separation between the valvulae conniventes which are of normal thickness despite dilatation of the bowel lumen.

Although the term hide-bound is used specifically to describe scleroderma, the same appearance may also be seen in sprue. The stack of coins sign, although similar, should not be confused with the hide-bound sign. The former is seen in intramural haematoma as adjacent, thickened folds with sharp demarcation and crowding of the valvulae conniventes.

Pathology

The cause of hidebound appearance in scleroderma is thought to be asymmetric smooth muscle atrophy of the inner circular muscularis layer relative to the outer longitudinal layer. Contraction of the longitudinal layer results in foreshortening of the bowel and close packing of the valvulae conniventes.

History and etymology

The term hide-bound sign was coined by Alfred Horowitz and Morton Meyers in a study published in 1973, although according to their article the appearance had been described prior to that 3. The term hide-bound was originally used to describe emaciated cattle.

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21
Q

What is Whipple Disease?

A
  • Rare multisystem disease
  • Tropheryma Whippelii
  • Involves
    • SIJ
    • joint capsule
    • heart valves
    • CNS
    • Jejunum
  • Clinical
    • middle aged men, USA and North europe
    • Diarrhea, steatorrhea
    • Immune defects
  • Imaging
    • 1-2mm diffuse micronodules in jejunum
    • no dilation or increased secrions
    • Nodal masses in mesentery
    • nodes have low CT density and are echogenic on USS
    • sacroiliac.
  • BUZZ WORDS
    • intestinal lipdystrophy
    • sand like nodules
    • low density nodes on CT
    • rare
    • Multi-system
    • Tropheryma Whippelii

Whipple disease (gastrointestinal manifestations)

Dr Hamish Smith◉ and Dr A Tachibana et al.

Gastrointestinal manifestations are a key component of Whipple disease. The gastrointestinal manifestations of Tropheryma whipplei are also known as intestinal lipodystrophy.

Pathology

Extensive infiltration of the lamina propria with large macrophages infected by intracellular T. whipplei causes marked swelling of intestinal villi and thickened irregular mucosal folds primarily in the duodenum and proximal jejunum.

When they become large enough to be macroscopically visible, they may appear as innumerable small filling defects superimposed on irregularly thickened folds (sand-like nodules)

Radiographic features

Reported radiologic features include:

diffuse 1-2 mm micronodules (“sand-like nodules”) in the jejunum

thickened mucosal folds: especially the jejunum

small bowel calibre: normal or slightly dilated

mesenteric lymphadenopathy: nodes of very low (near fat) density 2

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22
Q

In what diseases are Enteric fistulas seen?

A
  • Fistulas of the SB with adjacent struts can be seen with Crohn Disease, CRC, post op and in diverticular disease.
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23
Q

Drug Chemotherapy induced enteritis

A
  • GI edema
  • necrosis
  • perforation
  • most common in long term immunosuppered pts to prevent homograft rejection or pts getting chemo for leukaemia or lymphoma
  • CT findings can be seen in diseased or undiseased segments of bowel.
  • IMAGING FINDIGNS:
    • nonspecific focal or diffuse bowel wall thcikening with or without the target sign or as regional mesenteric vascular engorement and haziness more often in distal SB
  • DDx
    • ACE inhibitors may cause angioedema resulting in reversible wall thickening.
  • Figure 11a: Irinotecan-induced enteritis. Patient with recurrent metastatic colorectal cancer developed abdominal pain and constipation 2 months after initiation of chemotherapy regimen containing irinotecan. (a) Axial contrast-enhanced CT image reveals mild small-bowel wall thickening and dilatation. (b) Upper gastrointestinal tract series demonstrates terminal ileitis with featureless small bowel and loss of normal fold pattern.
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24
Q

In which patient group does cryptosporidiosis infectious enteritis occur?

A
  • Cryptosporidium species are protozoa that frequently cause enteritis in AIDs patients and rarely in immunocompetent patients
  • Imaging features
    • thickened SB folds
    • SB dilatation

https://www.ajronline.org/doi/pdf/10.2214/ajr.143.3.549

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25
Q

Parasitic Infectious enteritis

3

A
  • hookworm
    • Thickened folds
    • nodulatity
  • tape worm
    • filling defect in bowel
  • Ascaris
    • Filling defect
    • intestinal obstruction
    • Ascaris lumbricoides (roundworm)
    • Most common helminthic infestation in the world
    • Usually asymptomatic and most common in children ages 1 to 10 years
    • Most often found in distal small bowel
    • Life cycle
      • Infection is through contaminated soil
      • Involves GI tract of host twice
      • First time as egg
      • Migrates through lungs
      • Adult travels up trachea
      • Returns to GI tract for maturation (2 months)
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26
Q

Infectious/bacterial causes of infectious enteritis

5

A
  • Yersina enterocolitica
    • thickened folds
    • nodularity
    • terminal ileum
    • ulcers
  • TB
    • Strictures
    • Obstruction
    • Terminal ilium
  • Histosplasmosis
    • thickened folds
    • Nodularity
  • Salmonellosis
    • Thickened folds
    • nodularity
    • Terminal ilium
  • campylobacter
    • Thickened folds
    • Nodularity
    • loss of haystration
    • Terminal ilium
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27
Q

bowel infections common in AIDS

5

A
  • CMV
    • Thickened folds in Caecum
    • pancolitis
  • TB
    • Thicken folds in caeum
    • Adenopathy with low central attenuaiton
    • Terminal ileum
  • MAI
    • THickened folds
    • nodularity
    • adenopathy
  • Cryptosporidiosis
    • Thickened folds
  • Giardiasis
    • Thickened folds
    • largely jejunal
    • jejunal spasm.

Introduction Cryptosporidiosis has been recognised as an opportunistic infection of the bile ducts since 1972 when Kovatch and White described cryptosporidial cholangitis in juvenile rhesus monkeys.’ In 1983 the first cases of hepatobiliary cryptosporidiosis in patients with AIDS were reported.23 It was suggested that the gall bladder was the source of the bile duct infections. Soon after this, infection of the biliary tree by cytomegalovirus (CMV) was described, both in association with cryptosporidial infection and on its own.45 Several papers describing the pathological findings in the biliary tract in patients with AIDS have now been published. Most of these include only small numbers of patients and it remains difficult to form an impression of the incidence of clinical disease in the biliary tree and the range of pathological findings.67 Material from the gall bladder and biliary tree is usually difficult to obtain. In the largest published study, reviewed by Cello (1992), out of 40 patients with bile duct disease 18 had a specific histopathological diagnosis.8 The diagnoses were based on biopsy specimens taken from the ampulla of Vater or post mortem findings. The commonest diagnoses made were CMV (eight cases) and cryptosporidium (six cases). Other specific diagnoses included Mycobacterium avium (three cases), Kaposi’s sarcoma (one case) and lymphoma (one case). The remaining 22 cases all showed inflammatory changes. Department of Histopathology, St Mary’s Hospital Medical School, Imperial College of Science, Technology and Medicine, London W2 IPG R D Goldin Department of Medicine J Hunt Correspondence to: Dr R D Goldin Accepted for publication 20 January 1993 Cytomegalovirus This is one of the commonest organisms in patients with AIDS and frequently affects the liver and biliary tree. It is usually part of a disseminated disease: cholestatic liver function tests have been reported in one third of patients and radiological evidence of sclerosing cholangitis in 3-11%.9 In the case of the biliary tree viral inclusions do not always have the characteristic owl’s eye appearance and immunohistochemistry for CMV is extremely useful in doubtful cases. Cryptosporidial infection Cryptosporidial infection is a common cause of diarrhoea in patients with and without AIDS.10 Biliary tract disease, however has only been seen in patients with AIDS.” Biliary tract abnormalities have been described in 10% of patients with intestinal cryptosporidiosis.”I The organism is a sporozoa and undergoes its complete life cycle within a single host making reinfection a possibility.’2 In the bile ducts and intestines the organism is seen as small, round, basophilic structures on the luminal surface, 2-4 ,um in size. Although they can usually be seen easily in haemotoxylin and eosin stained sections, a Giemsa stain has been recommended. Cryptosporidial infection is associated with little inflammation, although in the bowel it has been claimed that there is an increased number of apoptotic bodies. Surprisingly, “an exuberant inflammatory reaction” has been described in association with biliary tract cryptosporidiosis in one study.”3 The electron microscopic appearance of the organism is characteristic but is not necessary for diagnostic purposes. A potentially important preliminary observation is that there is electron microscopic evidence of autonomic nerve damage in the bowel and it has been suggested that this may cause disordered motility.’4 A corresponding abnormality may be found in the biliary tree. Mycobacterium avium intracellulare Mycobacterial infections are also very common in patients with AIDS and have been identified in duodenal or ampullary biopsy specimens in a number of patients with bile duct disease.8 These have usually been caused by M avium intracellulare. As in other parts of the body these are frequently found in large numbers in poorly formed granulomas and are both Ziehl Neelson and periodic acid Schiff positive. Microsporidial infection Microsporidia are diverse phyla. Infection by members of this group is extremely rare in patients who do not have AIDS. Enterocytozoon bienusi has mainly been associated with intestinal infection and diarrhoea’5 but microsporidia have been associated with peritonitis and granulomatous hepatitis.’6 It has also been found associated with sclerosing cholangitis and its importance has probably been underestimated.’7-20 This has been confirmed by a recent study in which the diagnosis was made in eight patients with AIDS who had unexplained cholangitis.2’ In all eight patients the organism was detected by staining bile samples, in six it was detected in duodenal biopsy specimens. Diagnosis of infection by these organisms requires active consideration by the histopathologist and electron microscopy is useful, although light microscopy is often diagnostic.22 691 on February 8, 2022 by guest. Protected by copyright. http://jcp.bmj.com/ J Clin Pathol: first published as 10.1136/jcp.46.8.691 on 1 August 1993. Downloaded from Goldin, Hunt Lymphomas Lymphoma in patients with AIDS often affects extranodal sites.2’ Primary lymphomas of the gall bladder,’24 common bile duct,’25 and head of pancreas26 have been recognised, although this is much less common in disseminated disease. All these reported tumours have been high grade B cell lymphomas ranging from Burkitt-like to immunoblastic tumours. Disease in the gall bladder has so far been asymptomatic; tumours of the bile ducts and the head of the pancreas have presented early with asymptomatic jaundice.’6 Kaposi’s sarcoma As is the case in the liver, disease of the gall bladder and biliary tree is seen at necropsy as part of widespread disease, although it rarely presents as a clinical problem.28 29 Kaposi’s sarcoma involving the common bile duct, however, has been associated with cholangitis and jaundice.’7 This may also follow on from extensive disease of the hepatic hilum with compression of the main bile ducts.’0 Clinical and radiological findings Gastrointestinal symptoms are common in AIDS,”3 and patients may present with dysphagia, diarrhoea, or abdominal pain. In patients with right upper quadrant pain the clinician should suspect bilary disease.” ‘34 In one study of 64 patients with AIDS and abdominal pain the site was the right upper quadrant in 27, and of these 17 had biliary disease.35 The pain may have been due to acalculous cholecystitis, in which CMV, cryptosporidium, and campylobacter have been implicated,4 or AIDS related sclerosing cholangitis. In the latter serum alkaline phosphatase is often several times above normal, suggesting cholestasis.” In a third of cases, however, the serum liver function tests are normal35 and jaundice is rarely seen.33 36 The imaging features of AIDS related cholangitis are dilatation and irregularity of either the intrahepatic or extrahepatic ducts. An ultrasound scan may show intrahepatic and extrahepatic bile duct dilatation or irregularity of both the diameter of the intrahepatic ducts and the common bile duct wall, or periductular hyperechoic regions in the liver.”3 33 37 Thickening of the gall bladder wall, due to acalculous cholecystitis, can be detected38 and the pancreatic duct may also be dilated. The sensitivity of ultrasound scanning varies from 100%37 to 70%,36 while the specificity approaches 85%.36 Computed tomography has not been extensively assessed but may be better than ultrasound scanning for detection of intrahepatic disease.” Endoscopic retrograde cholangiopancreatography (ERCP) is the optimal diagnostic technique.13 323435 At ERCP four abnormal cholangiographic patterns are discernible.’6 The commonest is sclerosing cholangitis with ampullary stenosis in which both irregularity of the intrahepatic ducts and dilatation of the common bile duct down to the level of the ampulla are evident, with delay in drainage of contrast. Alternatively, isolated ampullary stenosis may be seen when the common bile duct is dilated but the intrahepatic ducts are not stenosed. Similarly, intrahepatic sclerosing cholangitis or extrahepatic biliary strictures may each appear in isolation. In many cases subtle changes occur in the wall of the common bile duct which looks beaded and irregular.39 More than half the patients studied have evidence of ampullary stenosis.33 3 Biopsy specimens of both the ampulla and bile duct can be taken at ERCP and sphincterotomy performed if indicated.3 Because of the design of the biopsy forceps, ampullary cannulation has been difficult and biliary biopsy tends only to be performed after removal of the sphincter. Duodenal and ampullary biopsy specimens were used as surrogates for biliary epithelium and biliary brush cytology specimens taken. Unfortunately, cytology has not proved diagnostic.35 Recently Teflon coated, swivel-tipped, rat toothed biopsy forceps have been marketed (Olympus FB-39Q or FB-40Q). These can be passed down the duodenoscope into the biliary tree through an intact ampulla. They are radio-opaque and incorporate a contrast injection channel and allow targeted biopsy specimens to be taken. The increased use of these forceps will advance the description of biliary pathology. Biopsy specimens from the ampulla and juxta-ampullary bile duct after sphincterotomy have shown CMV and cryptosporidium infection in 11%-25% and 25-35% of cases.’5’6 But these agents are also seen, albeit less frequently, in those without ampullary stenosis. 13 Microsporidial infection17 18 and Candida Sp40 have also been found in the biliary epithelium of these patients, but in 50% of patients a cause for the stenosis is not established. M avium intracellulare has been found in duodenal biopsy specimens. The prognosis of AIDS related sclerosing cholangitis is poor. In the largest series 40% of the patients died within nine months, although biliary disease did not appear to be the cause.’6 There have been two recent studies on related sclerosing cholangitis.’0 41 In the first of these, out of the 20 cases examined, 13 had cryptosporidiosis and six had active CMV infections. Compared with controls the overall survival was no worse (median 7-5 months). Surprisingly, increased age seemed to be protective in AIDS related sclerosing cholangitis. The overall findings in the second study were similar. There was a single case of microsporidial infection. The importance of actively considering the diagnosis of microsporidial infection in patients with AIDS and unexplained sclerosing cholangitis has been borne out in another recent paper.2’ In eight patients with AIDS and unexplained cholangitis this diagnosis was made after thorough examination of the biliary tree.

https://jcp.bmj.com/content/jclinpath/46/8/691.full.pdf

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28
Q

what is this?

A
  • Ascariasis/round worm infection
    • most common parasitic infection world wide
    • GIT
      • Jejunum>ileum, duodenum, stomach
      • visible on SBFT as longitudinal filling defects
      • enteric canal of worm is filled with barium
      • Worms may cluster ‘bolus of worms’
      • can cause SBO
      • Perforation volvulus
    • Bilary tract
      • intermittent biliary obstruction
      • granulomatous stricture of the bile duct (rare)
      • Oriental cholangiohepatitis.
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29
Q

which cell type does this tumour arise from?

Most common Locations?

Symtoms of this tumour in the GIT ?

A
  • carcinoid tumors arise from enterochromaffin cells
  • Location
    • GIT 85%
      • appendix 50%
      • SB 33%
        • 90% distal ileum
        • 30% SB carcinoids are multiple
        • 40-80% spread to mesentary
      • Gastic, colon, rectum 2%
    • Bronchial Tree 15%
    • Rare locations
      • thyroid
      • Teratomas
        • ovarian
        • testicular
  • Symptoms of GI carcinoids
    • 70% asymptomatic
    • 20% obstruction
    • 15% weight loss
    • 15% mass
  • Case courtesy of Dr Bruno Di Muzio, Radiopaedia.org, rID: 19593
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30
Q

In patients with carcinoid syndrome, what stage disease/where is their disease?

What symptoms do they have?

What substances does the tumour produce?

A
  • In patients with carcinoid syndrome, what stage disease/where is their disease?
    • 90% have liver mets
  • What symptoms do they have?
    • recurrent diarrhea 70%
    • right sided endocardial fibroelastosis
      • tricuspid insufficiency
      • pulmonary valve stenosis
    • The left side of the heart is spared bc/of metabolism by monoamine oxidase inhibitor (MAOi) in the lung
    • Wheezing bronchospasm
    • Flushing of face and neck
  • What substances does the tumour produce?
    • ACTH
    • Histamine
    • bradykinin
    • Kallikrein
    • serotonin (excreted as 5-HIAA in urine)
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31
Q

complications of Carcinoid syndrome

3

A
  • ischaemia with mesenteric venous compromise
  • hemorrhage
  • malignant degeneration
    • gastric and appendicieal tumours rarely metastazie
    • SB tumours met commonly
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32
Q

Imaging features of Carcinoid tumors/syndrome

A
  • Mass in SB/filling defect
  • strong desmoplastic reaction causes angulation, kinking of bowel loops (tethered appearance)
  • mesenteric venous congestion
  • mesenteric mass on CT with spoke wheel pattern is virtually pathognomonic with the only other disease to cause this being retractile mesenteritis (very rare)
  • Stipple calcification in mesenteric mass
  • obstruction secondary to desoplastic reaction
  • VEry vascular tumours
    • tumour blush at angiography
    • very hyperintense on T2W imaging
    • Liver mets (art phase indicated)
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33
Q

Which organs have the highest to lowest tolerance to radiation/radiation enteritis?

What is the tolerance Dose?

A
  • highest to lowest tolerance
    • duodenum
    • jejunum
    • ileum
    • transverse colon
    • sigmoid colon
    • oesophagus
    • rectum
  • Radiation entertisis is damage of SB mucosa and wall as a result of therapeutic radiation
  • Tolerance dose (TD 5/5) is the total dose that produces radiation damage in 5% of pts within 5 years
    • TD5/5 is 4500cGy in SB and colon
    • 5000cGy in rectum
  • Imaging
    • mural thickening and luminal narrowing usually in pelvic bowel loops
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34
Q

what is this condition?

which medicine have they been started on?

A
  • ace inhibitor related angioedema
    • acute onset or recurrent acute abdominal pain
    • segmental area of circumferential bowel wall thicekning
    • decreased submucosal attenutation
    • mesenteric edema
    • ascties
    • engorgement of the vasa recta
  • Case courtesy of Dr Michael P Hartung, Radiopaedia.org, rID: 88116
  • Case Discussion

This patient presented with severe abdominal pain, and had concern of ischemia from the first CT and proceeded to exploratory surgery with negative results. The patient’s pain continued for more than a month before repeating the imaging with worsening inflammation, prompting the suggested diagnosis of ACE-inhibitor-related angioedema. After this suggestion, the medication was stopped and the patient’s symptoms rapidly improved, with resolution of bowel wall thickening at the final follow-up scan.

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35
Q

What is glucagon and what effects does it ahve on the body?

What are the contraindications to administering Glucagon?

A
  • 29 amnio acid peptide produced in alpha cells of the pancreas
  • Stimulus for release is hynger/hypoglycaemia
  • Effects
    • antagonist to insulin -> increases BSL
    • relaxation of smooth muscle cells
    • Relaxation of GB sphincter and sphincter of oddi increasing bile flow.
  • Useful in Barium enema or when ever smooth smucle spasm is suspected of producing a pseudostenotic lesion.
  • it can be used in eval of the oesophagus, stomach, duodenum, small intestine, CBD and colon.
  • Contraindications include
    • phaeochromocytoma
    • insulinoma
    • glaucoma
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36
Q

CT Colonography uses, technique

A
  • replacing DCBE for dectecting and screening of colonic neoplasms
  • helically acquired axial imagins of the gas distended colon are obtained during breath holding in both prode and supine positions
  • Images are combined into a detailed model of the colon and viewed on 2D multiplanar recons or primary 3D endoluminal display.
  • Standard CTColonography does not use IV contrast and uses low does 20% dose of standard CT and 10% less than a DCBE.
  • Dectection of large polyps >10mm and polyps 6-9mm is comparable/equal to optical colonoscopy.
  • Optical colonoscopy is better for polyps <6mm.
  • sensitivity 92% >10mm and per patient specitificy 96%
  • Requires bowel prep similar to colonoscopy.
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37
Q

MRE

use

pros

cons

fibrotic findings

inflammatory findings

A
  • eval of SB and LB in pts with IBD
  • depicts extraluminal abnormalities
  • can distinguish active from fibrotic strictures and can delineate fistulas
  • no ratdiation
  • long acquisition times
  • difficult to identify early mucosal lesions.
  • Imaging findings
    • Fibrosis
      • Low t2 sig in a thickened loop
      • delayed enhancement
    • acute inflammatory findings
      • wall thickening
      • early mucosal enphancement
      • engorgement of the vasa recta
      • diffusion restriction in the wall.
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38
Q

What is the most common polyp type in the bowel?

A
  • non-neoplastic hyperplastic polyps are the most frequent type of polyp.
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39
Q

Non-neoplastic polyps

single

multiple -> syndromes

A
  • hamartomas
    • single -> hamatoma
    • Multiple
      • Cronkhite-Canada syndrome
      • Juvenile polposis
      • Peutz-Jeghers syndrome
  • Inflammatory
    • single
      • benign lymphoid polyp
      • fibroid granulation polyp
    • multiple
      • juvenile polyp
      • benign lymphoid polyp
      • Granulomatous colitis
  • Unclassified
    • single
      • hyperplastic polyp
    • Multiple
      • hyperplastic polyposis
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40
Q

what is the ddx for this condition

A

Axial T2 HASTE

MR ENTEROGRAPHY

There are innumerable polyps in the stomach and first part of duodenum of varying size and morphology, most numerous in the distal body and antrum of the stomach where they are confluent and “carpeting” the gastric mucosa. Sparing of the gastric fundus.

The gastroduodenal polyps demonstrate moderately hyperintense signal and have a smoothly lobulated, frond-like outline with no obvious extension through the gastric wall

Appearances favour a polyposis syndrome, including Peutz-Jeghers, Cowden, Cronkhite-Canada or juvenile polyposis syndrome. Absence of polyps in the fundus makes familial adenomatous polyposis less likely.

Cronkhite-Canada syndrome is a type of non-neoplastic, non-hereditary hamartomatous polyposis syndrome characterised by rash, alopecia, and watery diarrhoea.

Epidemiology

There is a recognised male predilection with 3:2 male:female. Patients typically are middle age (50-60 years of age) 1. 75% of the approximate 500 cases in the literature were from Japan 7.

Clinical presentation

Patients typically present with watery diarrhoea and a protein-losing enteropathy with associated nail atrophy, brownish skin pigmentation, and alopecia 3.

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41
Q

Neoplastic Polyps

single

multiple

A
  • Epithelial
    • single
      • Tubular adenoma
      • tubulovillous adenomal
      • villous adenoma
      • turcot syndrome
    • Multiple
      • familial polyposis
      • Gardener syndrome
  • Non-epithelial
    • carcinoid
    • leiomyoma
    • lipma
    • fibroma
42
Q

Adenomatous Polyps

How common?

Types? 3

Location

A
  • Most common true colonic tumour
  • found in 10% of pop by the 7th decade
  • 50% are multiple
  • Clinical findings
    • pain haeimorrage
  • Types
    • tubular (most common)
    • tubulovillous
    • villious (least common)
  • Location
    • rectum and sigmoid 60%
    • Descending colon15%
    • trans colon 15%
    • ascending colon 10%
43
Q

features of benign vs malignant polyps

A
  • Benign
    • <1cm
    • Stalk present
    • smooth
    • signle
    • smooth
  • Malignant
    • >2cm
    • no stalk instead appears sessile
    • contour is irregular/lobulared
    • multiple
    • indented, retracted
  • histologic differentiation of polyps is invariably difficult radiographically so the majority of lesions require endoscopic sampling.
44
Q

what is an advanced adenoma?

A
  • polyp > 1cm
  • high grade dysplasia
  • of all the polyps <1cm, the likely ook that is lesion is an advanced adenoma is 3%
  • the majority are hyperplastic and the rest are bengn adenomas
45
Q

What is a hyperplastic polyp?

A
  • focal proliferation of normal mucosa, therefore not an adenoma
  • no malignant potential
  • due to excessive cellular proliferation in Lieberkuhn crypts
  • 75% of polyps occur distal to the splenic flexure. Mostly in the rectosigmoid area
  • imaging features
    • stalked polup
    • sessile <5mm
46
Q

What is Postinflammatory polyps/polyposis?

A
  • Postinflammatory polyposis (PIPs, pseudopolyposis, filiform polyps)
  • benign condition
  • not a/w cancer
  • occur most commonly in Crophn disease and UC secondary to regeneration of nonulcerated tissue.
  • Filiform polyps are thin, short branching structures.
47
Q

how to differentiate true polyps from pseudopolyps

A
  • Polyp
    • uniform in size
    • round, stalked sessile
    • well delineated
    • preserved colonic haustra
  • Pseudopolyp
    • uniform in size
    • y-shaped, filiform, irregular
    • fuzzy margins (inflammation)
    • distorted colonic haustra (inflammation)
48
Q

Name 6 polyposis Syndromes

A
  1. Familial polyposis
  2. Gardner syndrome
  3. Peutz-Jeghers syndrome
  4. Juvenile polypsosis
  5. Cowden disease
  6. Turcot syndrome
49
Q

What is the most common intestinal polyposis syndrome?

A

Familial polyposis. 1:8000

50
Q

Familial Polyposis

age of malignant degeneration

treatment

how many polyps

when should screening start?

A
  • Screening of family members of familial polyposis patients should start at puberty
  • malignant degeneration by 40 years old
  • treatment is propholatictc total proctocolectomy
  • usually >100 polyps
  • Familial adenomatous polyposis syndrome is a common umbrella name under which
    • gardner and
    • familial polyposis syndrome
51
Q

Name that syndrome

Intestinal polyps

osteomas

soft tissue tumors

sarcomas

ampullary ca

ovarian ca

A

Gardner Syndrome

  • Polyposis
    • 100% colon
    • duodenum 90%
  • hamartomas of the stomach
  • soft tissue tumours
    • inclusion cysts
    • desmoids
    • fibrosis
  • oesteoma in the calvarium, mandible sinuses
  • entrapment of cranial nerves
  • malignant transformation in 100% if left untreated
  • SB and pancreaticoduodenal maligannces
  • total colectomy recommended.
  • PATHOLOGY
    • There is an autosomal dominant inheritance in the FAP gene (chromosome 5q) in a majority of patients but with 20% of cases resulting from new mutations. Extracolonic features often precede the diagnosis of colonic polyps.
52
Q

Name that syndrome

second most common intestinal polyposis

autosomal dominant

hamatomas throughout GIT (except Oesophagus)

Mucocutaneous pigmentations (buccal mucosa, palm, sole)

Polyps have little malignant potential

increased risk of stomach, duodenal and ovarian ca.

benign neoplasm of testes, thyroid and GU system.

A
  • Peutz-Jeghers Syndrome
  • Pathology

Peutz-Jeghers polyps are non-neoplastic hamartomas due to the proliferation of all three layers of the mucosa, which have a characteristic feature of a smooth muscle core continuous with muscularis mucosa in a tree-like branching pattern.

  • This distinguishes them from the hamartomatous polyps of Cronkhite-Canada syndrome, juvenile polyposis and Cowden disease 1.
53
Q

Describhe the pathology of peutz jeghers syndrome

A

polyps are non-neoplastic hamartomas

due to the proliferation of all three layers of the mucosa,

which have a characteristic feature of a smooth muscle core continuous with muscularis mucosa in a tree-like branching pattern.

This distinguishes them from the hamartomatous polyps of Cronkhite-Canada syndrome, juvenile polyposis and Cowden disease 1.

54
Q

What are patients with PJS at increased risk of?

A

Patients are at increased risk of:

  • intussusception
  • GI tract adenocarcinoma, although the polyps themselves are not premalignant
    • stomach: 29% lifetime risk 4​
    • small intestine: 13% lifetime risk 4
  • extraintestinal malignancies
    • adenoma malignum (adenocarcinoma subtype of the cervix)
    • breast: 45-50% lifetime risk 4, more frequently ductal
    • pancreas: 11-36% lifetime risk 4
    • ovary: 18-21% lifetime risk 4, mainly sex cord tumours
    • uterus: 9-10% lifetime risk 4
    • cervix: 10-23% lifetime risk 4
    • testis: 9% lifetime risk 4, large calcifying Sertoli cell tumours
    • lung: 15-17% lifetime risk 4
55
Q

Name that syndrome

large polyps in rectum

present in children with bleeding, prolapse or obstricition

A

Juvenile polyposis

  • AD
  • 100% have colon polyps
  • Presentation in the second decade is most common 2.
  • Juvenile polyposis syndrome is characterised by the presence of hundreds of hamartomatous polyps containing fluid/mucus.
  • Both the tumour suppressor gene SMAD4 on chromosome 10q (50% of cases) and BMPR1A gene have been implicated. The genetic basis is not always known 1.
  • Associations
    • Other congenital abnormalities are present in 20% of patients 1,2:
      • intestinal malrotation
      • Meckel diverticulum
      • hydrocephalus
      • congenital heart disease
      • mesenteric lymphangioma
      • pulmonary arteriovenous malformation
56
Q

Name that Syndrome

Multiple hamatomas

mucocunatous pigmentations

thyroid gland abnormalities

breast cancer (ductal)

Uterine and cervical cas

TCC of the bladder and ureter

which syndromes is this syndrome associated with?

A
  • Cowden syndrome
    • Multiple Hamartoma syndrome of the bowel/GIT
    • Fibrocystic change of the breast
    • Thyroid changes
    • mucocutaneous lesions
    • Increased risk of:
      • breast ca
      • Thyroid ca
      • CNS: dysplastic cerebellar gangliocytoma, occurs when in association with Lhermitte-Duclos disease (LDD)
  • Syndromic associations

Cowden syndrome is part of a group of disease known as PTEN-related diseases, which also includes:

Lhermitte-Duclos disease (LDD)

Bannayan-Riley-Ruvalcaba syndrome (BRRS) 3

  • https://www.ajronline.org/doi/pdf/10.2214/ajr.135.2.385
57
Q

Name that syndrome

  • Autosomal Recessive
  • glioma
  • medulloblastomas
  • Colonic adenomas

Describe the genetics of the syndrome

A

Turcot syndrome

Dr Ammar Haouimi◉ and Assoc Prof Frank Gaillard◉◈ et al.

Turcot syndrome is one of the variations in polyposis syndromes. It is characterised by multiple colonic polyps and an increased risk of colon and primary brain cancers.

Epidemiology

Turcot syndrome is a rare disease. Patients typically present in the second decade 3.

Pathology

Turcot syndrome is characterised by:

intestinal polyposis

CNS tumours: most commonly glioblastoma or medulloblastoma

Genetics

It is thought to carry an autosomal recessive inheritance. Two-thirds of patients have mutations in the APC gene, the same genetic defect as in familial adenomatous polyposis (FAP). These patients have multiple colonic adenomas, and virtually all develop colorectal carcinoma by the age of 40. The common intracranial tumour in this subtype is medulloblastoma.

The other third have mutations in the HNPCC genes. Colonic malignancy is not as common in this type but tends to develop at a younger age. Most develop glioblastomas.

58
Q

Modifiable risk factors for colon cancer

A
  • being overweight/obese
  • inactivity
  • diets high in red meat
  • diets low in fruits and veg
  • smoking
  • heavy alcohol use
59
Q

nonmodifiable colon cancer risk factors

A
  • personal hx of CRC or adenomatous polyps
  • personal hx of chronic IBD
  • Strong fhx of CRC or polyps
    • cancer or polyps in a first degree relative <60yo
    • or in 2 first degree relative of any age
  • older age
  • aftrican american
  • Ashkenazi Jewish descent
60
Q

Most common location for CRC

A
  • Rectum 35%
  • sigmoid 25%
  • Descening colon10%
  • ascending colon 10%
  • trasnsverse colon 10%
  • cecum 10%
61
Q

name the 5 different appearances of CRC

A
  • PAPUS
    • Plaque-like (cloacogenic tumour at anorectal junction
    • Annular/applecore (<5cm long)
    • Polyp
    • Ulcerative
    • Scirrhous (rare: long >5cm circumferential spread)
      *
62
Q

name 5 complications of CRC

A

Complications

  1. Obstruction
  2. intussusception (in polyploid lesions - rare)
  3. Local perforation (simulates diverticulitis)
  4. Local tumor recurrence
  5. Peritoneal spread
63
Q

What is the name of CRC Staging?

describe the staging and 5ys

A
  • Dukes staging system
    • Dukes A
      • limited to bowel wall
      • 15%
      • 93% 5ys
    • Dukes B
      • extension into serosa or mesenteric fat
      • 35%
      • 77% 5ys
    • Dukes C
      • LN mets
      • 35%
      • 48% 5ys
    • Dukes D
      • distant Mets 15%
      • 7% 5ys
64
Q

Describe the T component of the TNM Staging of CRC

A
  • Tx
    • no description of the tumors extent is possible
  • Tis
    • cancer in the earliest stage.
    • has not grown beyond the mucosa (inner layer of the bowel)
    • carcinoma insitu.
  • T1
    • cancer has growth through the mucosa and extends into the submucosa
  • T2
    • Cancer has grown through the submucosa and extends into the muscularis propria
  • T3
    • Cancer has grown thru the muscularis propria into the serosa but not into organs or tissues
  • T4
    • Cancer has grown throught the wall of the bowel into near by tissues or organs
65
Q

Describe the N and M component of the TNM Staging of CRC

A
  • N0
    • no LN involvement
  • N1
    • cancer in 1-3 near by LNs
  • N2
    • Cancer in 4 or more near by LNs
  • Mx
    • no description of distant spread is possible bc of incmompleted information
  • M0
    • no distant spread is seen
  • M1
    • distant spread is present.
66
Q

Name the layers of the bowel wall

A
  • MSMS
    • Mucosa
    • Submucosa
    • Muscularis Propria
    • Serosa
67
Q

What is the diagnostic accuracy of CT detection of LN and Liver mets in CRC?

A
  • LN Mets on CT
    • 50-70%
  • Liver mets
    • 60-70% on CECT
    • 70-80% on MRI
68
Q

What is the purpose of rectal MRI?

Which LNs denote M1 disease

what defines T3 disease?

A
  • used to stage and differentiate T2 from T3 disease
    • T3 disease requires neoadjuvant chemorads before surgery
  • T2W is the most reliable sequence for local staging
  • can have desmoplastic reaction with linear T2 hypointensity in T2 disease
  • T3:
    • nodular extension of T2 intermediate tumour outside of the Muscularis propria to clam T3 disease
  • must closely evaluate the external iliac Lns as these denote M1 (distant metastatic disease) in Rectal Ca.
69
Q

Name 4 broad categories of COlitis

A
  • inflammatory
    • CD
    • UC
    • Behcets
  • ischaemic
  • infectious
  • Iatrogenic
    • chemo
    • rads
70
Q

Imaging features of mucosal inflammation re Colitis

which type of colits is demonstrated in this picture?

A
  • Ulceration
    • granulatiry of mucosa, apththoid
    • flask like collections of barium. collar button.
  • edema
    • displacement of barium:
      • translucent halo around central ulcer
  • Spasm
    • localised persistent contraction
    • narrowing of bwoel lumen
  • The whole colon, without skips is affected by an irregular mucosa with loss of normal haustral markings.

Case Discussion

Continuous lesion without skip,or carpeting of the whole colon is classic for ulcerative colitis.

Mucosal inflammation causes a granular appearance to the surface of the bowel. As inflammation increases, the bowel wall and haustra thicken. Mucosal ulcers are undermined (button-shaped ulcers). When most of the mucosa has been lost, islands of mucosa remain giving it a pseudo-polyp appearance.

A unique case from Prof. Saeed Rad, Tabriz, Iran.

71
Q
A

A Collar button-shaped benign ulcer on the lesser curvature of the stomach (AFIP Neg. #58-5294). B Low-power section through a benign gastric ulcer with a collar button shape showing mucosal undermining and superficial involvement of the muscular wall (AFIP Neg. ,//78-322) Collapse

72
Q

Rad features of Submucosal inflammation re Colitis

what sign is depicted here?

A
  • Ulcers
    • deeper linear than in mucosal inflammation
    • cobblestone appearance
  • Bowel wall thickening
    • CT
      • Wall thickened >3mm with lumen distended
    • Halo (in picture):
      • Fatty (chronic), gray (subacute or chronic), white (acute) with enhancement
    • Note the fat halo sign seen in the loop of small bowel anteriorly in both cross-section and longitudinally, representing submucosal fat deposition due to chronic inflammation. Case courtesy of Assoc Prof Frank Gaillard, Radiopaedia.org, rID: 2610
73
Q

Signs of Subserosal mesenteric inflammation re colitis

which sign is demonstrated?

A
  • stranding in surrounding fat
  • inflammatory mass
  • fistula
  • creeping fat:
    • excessive fat deposited around serosal surface (Crohn’s disease)
    • Creeping fat. Coronal SSFSE image demonstrates mesenteric fatty proliferation about the terminal ileum and sigmoid colon (arrows).
74
Q

what is Crohn’s Disease?

A
  • recurrent inflammatory condiof of the bowel caused by altered immunity to intestinal flora
  • lesions may occur in the enter GIT
  • most common in the
    • SB/TI - 80%
    • Colon - 70%
      • 25% of patients with colonic disease have pancolitis
    • Duodenum 25%
      *
75
Q

describe the pathologic development of lesions in Crohn’s disease

A
  • Initial event
  • hyperplasia of lymphoid tissue in submucosa
  • lymphedema
  • apthoid ulcerations
  • deeper ucers
  • fistulas
  • abscesses
  • strictures
76
Q

Imaging features of Crohn’s Disease

which sign is depicted?

A
  • fold thickening
  • nodular pattern
    • submucosal edema and inflammation
  • string sign
    • tubuar narrowing of intestinal lumen (edema, spasm, scarring depending on chronicity)
    • Case courtesy of Dr Ian Bickle, Radiopaedia.org, rID: 20855
    • Long segment of narrowed terminal ileum in a ‘string like’ configuration in keeping with a long stricture segment. Termed the string sign of Kantour (gastrointestinal string sign).
  • Omega sign
    • asymmetric wall involvement results in contracture and C-shaped loop on SB series
  • ram horn sign (second image)
    • loss of antral fornices with progressive narrowing from antrum to pyulous
77
Q

Describe the spatial arrangement of lesions in Crohn’s disease

A
  • Transitional zones are typical, they occure between involved bowel loops and normal bowel
  • Skip lesions are typical: discontinuous invovlemt of bowel
  • Lesions appear preferentially at mesenteric side of intestine.
78
Q

Extraintestinal Crohn’s Findings

A
  • Gall stones
  • ossess complications
    • spondylitis
    • sacroilitis
  • Steroid complications
    • Osteomyelitis
    • Osteoporosis
    • AVN
  • renal stones
79
Q

Primary intestinal findings of Crohn’s Disease

A
  • Bowel wall thickening
    • Normal is <3mm
    • mean diameter in CD is10mm
    • if >10mm
      • pseudomem colitis
      • ischemic
      • CMV colitis
  • Halo Sign:
    • Circumferential submucosal low attenuation surrounded by higher outer attenuation
  • Inner and out layers surrounding lower attenuation middle layer
    • target sign
  • Peribowel inflammation
    • dirty fat
    • ground glass
  • Mesentary
    • creeping fat
    • misty mesentery
    • SB adenopathy
    • Coming sign.
80
Q

Complications of Crohns’ Disease

A
  • Recurrence of disease after surgery
    • in contrast to UC in which proctocolectomy is curative
  • Increased incidence of ca.
    • GIT lumours
    • lymphoma
  • Toxic mega colon
  • fistulas
  • abscess formation
81
Q

Intro for Ulcerative Colitis

A
  • unknown cause
  • clinical findings include diarrhea and rectal bleeding
  • Disease affects primarily the mucosa (crypt abscesses) and typically starts in the rectum.
  • Ulcerative colitis (UC) is an inflammatory bowel disease (IBD) that not only predominantly affects the colon, but also has extraintestinal manifestations.
  • Epidemiology

Typically ulcerative colitis manifests in young adults (15-40 years of age) and is more prevalent in males but the onset of disease after age of 50 is also common 1,3,5

  • A combination of environmental and genetic factors are thought to play a role in the pathogenesis, although the condition remains idiopathic.
  • Ulcerative colitis is less prevalent in smokers than in non-smokers.
82
Q

Extraintestinal manifestations of UC

A
  • Joints
    • arthritis
    • arthralgia
    • ankspond
  • liver
    • sclerosing cholangitis
    • chronic active hepatitis
    • cholangiocarcinoma
  • skin
    • pyoderma gangrenosum
    • erythema nodosum
  • eyes
    • uveitis
    • episcleritis
83
Q

Imaging Features of Ulcerative Colitis

which sign is demonstrated?

A
  • Lead pipe colon
    • ahaustral
    • foreshortened colon
  • Granular mucosa
  • shallow confluent ulcerations
  • polyps
    • pseudopolyps
    • filiform polyps
      • regenerative mucosa
      • small thin, branching polyps
  • Spread
    • rectal disease first which is the worst
    • continuous spreat from distal to proximal colon
    • Circumfernetla bowel involvement
    • Backwash ileitis
      • only a short segment of TI unlike CD
      • Gaping ileocecal valve
  • Atypical imaging features
    • atypical patter of distribution
      • sparing. of the rectume 5% as it might be healting
    • crohn like findings:
      • discontinuous disease in 5-10% of patients
  • Mural and extramural findinsg
    • bowel wall thickening less than CD
    • distribuaiton from rectum continuously proximal
    • If pancolitis, TI may be affected for a very short length
    • Superimposed Ca:
      • Mass lesion or thick wall stricture
    • excessive fat surrounding rectosigmoid
      • creeping fat
    • Local LN enlargement
      • common in SB mesentery
      • infrequently in the retroperitoneum
84
Q

Complications of UC

Which sign is seen in this picture?

A
  • Toxic mega colon
    • ahaustral transverse coclon >6cm with pseudopolyps on kidney, urethra, bladder
  • Strictures
    • obstruction
    • can be benign or malignant
  • Malignancy
    • 5-30 fold increased risk
    • Annual incidence of 10% after the first decated
    • multiple in 25% of cases
    • often flat/scirrhous
85
Q

What is a perianal fistual?

what are the primary and secondary causes?

A
  • Abnormal connection between the epithelialized surface of the anal canal and the skin
  • causes
    • primary
      • obstruction of anal gland
      • stasis infection
      • fistula
    • secondary
      • iatrogenic (surgery)
      • Crohns
      • infection
      • malignancy
86
Q

4 types of Perianal Fistulas

A

PARKS CLASSIFICATION

  1. Intersphincteric (COMMON)
  2. transsphincteric (COMMON)
  3. Suprasphincteric
  4. Extrasphincteric (UNCOMMON seen inpts with multiple operations)
87
Q

How to report Fistulas

A
  • Mri is best
  • describe and classify type of fistula
  • Distance of mucosal defect to perianal skin
  • Secondary findings
    • abscesses
    • bowel wall abnormalities
    • reactive nodes
88
Q

What is a mimic of Crohn’s disease in the bowel?

A
  • Bechet disease
  • HLA B51 associated vasculitis
  • Intestinal manifestations
    • ulcers
    • strictures
    • fistulas
  • Extraintestinal manifesations
    • oral genital skin ulcers
    • uveitis
    • aneurysms
    • arthritis
  • Behc¸et syndrome is characterized by the histopathologic finding of nonspecific vasculitis in multiple organs. The diagnosis is usually made on the basis of the combination of clinical signs and symptoms. This disease involves the gastrointestinal tract in 10%–50% of patients, and the terminal ileum and cecum are chiefly affected. Barium study is useful in demonstrating the characteristic radiographic features of Behc¸et syndrome involving the gastrointestinal tract.
  • Behc¸et syndrome is a chronic, recurring, systemic disorder characterized by the histopathologic finding of nonspecific vasculitis in multiple organs. It primarily affects male patients between 11 and 30 years of age. This disease is found worldwide but has been reported to be most commonly seen in the countries of the eastern Mediterranean and the eastern rim of Asia (1,2); clinical features and gastrointestinal manifestations appear to be more common and more severe in Eastern patients than in North American and British patients (1). The prevalence has been reported to be 1 in 10,000 in Eastern countries (2) and 1 in 15,000 in North America (3).
89
Q

CMV COlitis

A
  • Occurs mainly in immun ocompromised hosts
  • imaging features
    • superficial or deep ulcers
    • thick wall >10mm
    • localised distribution in cecum, TI or Universal colitis
    • May be indistinguishable from psedomembranous colitis.
90
Q

What is Typhlitis?

A
  • AKA Neutropenic colitis
  • acutve necrotizing colitis involving the caecum, TI and/or ascending colon in pts with Leukaemia undergoing tx/immunosupression
  • unknown cause
    • leukemic bowel infiltration
    • intramural hemorrhage
    • bnecrosis
    • local ishemia
  • indications for Surgery
    • failed medical tx
    • perforation
    • hx
    • pericecal abscess and
    • uncontrolled sepsis
  • Clinical
    • RLQ pain
    • diarrhea
    • peritonitis
  • Imaging features
    • marked thickening of the cecum, tTI and or ascending colon
    • pericecal fluid and soft tissue stranding more marked than in pseudomembranous colitis
  • Complicaitons
    • perforation
    • pericolonic abscess pneumatosis
91
Q

What is Pseudomembranous colitis and what is it caused by.

when does it occur?

What are the imaging features?

what sign is depicted?

A
  • colitis caused by colonic overgrowth of C. difficile
  • 1-6 weeks after abx
  • Clincial findings
    • Diarrhea
    • fever
    • pain
    • leukocytosis
  • Imaging features
    • VEry thick haustral folds
    • thumb printing
    • ileus
    • very thick colonic wall
  • Accordion sign contrast between thickened folds
    • usually starts in rectum and progresses up
    • largely left sided disease
    • may be pancolitic
    • pericolonic fat changes in 35%
    • ascities in 35%
92
Q

what is amebiasis?

clinical symptoms

Where is it common?

Imaging features?

what sign is depicted

A
  • infection iwth Entamoeba histolytica
  • common in mexico sth americ, Africa, asia
  • Clinical
    • diarrhea
    • fever
    • may be asymptomatic for long persions
  • Transmission
    • person to person
    • contaminated food/water
  • imaging features
    • usually effects the cecum/right colon> transverse colon> recto sig.
    • Coned cecum
    • stenosis from healing and fibrosis
    • Ameboma
      • hyperplastic granuloma (1%)
    • Pericolic inflammation
    • fistula formation
  • intussusception sconday to ameboma in kids
  • liver abscess
  • pleuropulmonary abscess
  • brain abscess
  • cutaenosu extension (perianal)
93
Q

what is this?

A
94
Q

What are the different types of intestinal TB

What are the imaging features?

A
  • Primary intestinal TB
    • MAI (AIDS) - mycobacterium avium-intracellulare
    • M. Bovis (cows milk)
  • haematogenous spread from pulmonary TB
    • Caecum > colon > jejunum > Stomach
  • Imaging features
    • Stierlin sign
      • narrowed TI
      • marked bwoel wall thickening showrt segments
      • ulcers fissues fistulas strictures
      • Fleishner sign
        • marked hypertrophy of the ICv
        • Depicted
      • local adenopathy, may show low central density.
95
Q

what is this condition??

A
  • Colitis cystic profunda
  • beign lookalike disease characterised by submucosal, fluidfilled cysts
  • commonly in the rectum
  • cysts up to 3cm.
  • dx by histo to exclude malignancy (cystic mucinous adenoca.
96
Q

what is this condition? what is it caused by

which patient group?

how to diagnose?

A
  • Rectal lymphogranuloma venereum
  • caused by chlamydia tachomatis
  • sexually transmitted
  • Usually in MSM group
  • clincally
    • bleeding
  • purulent inflammation of the einguinal LNs occurs
  • Dx with the Frei intradermal test
97
Q

Definition of clonic diverticula

A
  • mucosal and submucosal outpouchings through the muscularis
  • mainly where vessels pierce the muscularis
    • ie btwn mesenteric and antimesenteric taenia
  • 95% sigmoid
  • performation causes diverticulitis
  • Clinically
    • pain fever bleeding
98
Q

Imaging features of diverticulitis

what sign is this?

A
  • extravasation of barium from tip of diverticulum -> microperf
  • free intraperitoneal air -> rare
  • intramural or paracolonic abscess
  • double tracking (intramural fistula) uncommon
  • fistula to bladder/uterus
  • muscular hypertrophy
99
Q

what is this?

A
  • isolated giant sigmoidal diverticulym
  • rare entity caused by a ball valve mechanism
  • large balloon-shaped gas-filled instruction in the lower abdomen located centrally in the pelvis
  • rare
  • important to differentiate it from a sigmoid or cecal volvulus
  • Complciations
    • divertifuotlis
    • SBO as a result of adhesions
    • perforation
    • volvulus of diverticulum
100
Q

In which patients is diverticulitis worse?

what may be masked by diverticulitis?

what is the recommendation?

A
  • pts on steroids predisposed to diverticulitis and worse disease
  • underlying ca may be obscured in pts > 50 years
  • endoscopic evaluation is indicated after resolution.