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					SPOT QUESTIONS 5
   (Sept 2004)‫‏‬
               Q1
Finding at gastroscopy

1. Describe this lesion
2. Diagnosis
3. Treatment
              Q2
48 year old woman with itchy
nipple

1. Diagnosis
2. Management
3. What operation would you do
to treat this?
               Q3


1. Diagnosis
2. Definition
3. How is it treated?
               Q4
Barium meal showing
extraluminal compression of
D2/D3. History of obstructive
jaundice, weight loss and back
pain in old man.

1. Most likely diagnosis?
2. Clinical findings?
3. Treatment options for the
diagnosis you have given.
               Q5
A healthy 84-year-old woman
with a 6-month history of a
slowly growing asymptomatic
lesion on the dorsum of her right
hand.

1. Diagnosis
2. Pathology
3. Natural history
4. Treatment
              Q6
Imaging finding:

1. Most likely diagnosis
2. Differential diagnosis
3. Pathogenesis most likely
4. Treatment
                 Q7
56yr female with previous
proctocolectomy.
1. Diagnosis
2. Natural history
3. Complications
4. Surveillance
               Q1
Finding at gastroscopy

1. Describe this lesion
2. Diagnosis
3. Treatment
   An ulcerated polypoid gastric lesion, appears to arise from
    submucosa with overlying normal mucosa
   GIST. Differential: atypical adenocarcinoma, MALT
    lymphoma, other lymphoma, other benign tumour
   Biopsy (“inkwell”, or in ulcerated region) – HISTO diagnosis by
    c-KIT (CD117), CD34, +/- actin staining [NB: -ve staining for
    desmin & S100]. EUS if available. Staging CT SCAN ABDO
    (direct spread, METS to liver and peritoneal cavity, lymph
    node spread is rare). Assessment of patient comorbidities.
    Discussion in UGI MDT meeting. Complete excision (R0
    resection). Imatinib for metastatic or unresectable disease
    (over 80% will respond). Discuss mutational testing for exon
    domain mutation (predicts reponse to Imatinib) and availability
    for adjuvant therapy with local Novartis drug rep. 3 monthly
    follow-up with 3-6mthly CT imaging.
   All GIST's have malignant potential. May occur anywhere from
    oesophagus to rectum (stomach 50-60%, small intestine 20-30%, colon
    5-10%, elsewhere ABDO cavity 5%, oesophagus 1.5%). Up to 30% are
    malignant at presentation, with 50% of these having metastasised. All
    have potential to become malignant. Post resection recurrence rates
    reported as high as 90%. Small intestinal GISTs are more aggressive
    than gastric GISTs of equal size. The most important prognostic features
    of primary tumour are: site, size, mitotic index, tumour rupture before or
    during surgery, complete resection margin. Up to 20% small GISTs
    (<5cm) exhibit metastatic behaviour, and very small lesions (<2cm) and
    those with a low mitotic activity can also metastasise. 80% of GISTs have
    a KIT tyrosine kinase mutation. Most affect exon 11 domain, however
    mutations also occur in exons 9,13,and 17. 5-7% occur as PDGFRA
    mutation. 10-15% are KIT and PDGFRA negative - “wild type” GISTs.
    Mutational analysis should be considered with primary disease,
    particularly those with high risk tumours. Kinase genotype can be
    determined from paraffin-embedded tumour samples.
   Imatinib (Glivec)‫‏‬
        Therapeutic effect can take several months (median
         3mths). Appropriate initial dose = 400mg daily
        Kinase genotype has predictive significance – KIT exon 11
         mutation was the single best predictor of a favourable
         response to Glivec
        Dose escalation if confirmed disease progression or
         documented exon 9 mutations. Check patient compliance
         first.
        Response to treatment determined by tumour size and
         density on CT scanning
48 year old woman with itchy
nipple‫‏‬

1. Diagnosis
2. Management
3. What operation would you do
to treat this?
   Paget's disease of the nipple.
   History and examination. Perform MAMMO and USS.
    Consider MRI (greater sensitivity) and may aid surgical
    planning. Confirm with full-thickness punch biopsy of the
    nipple. Exfoliative cytology or incisional biopsy if punch biopsy
    not available. Immunohistochemistry +ve staining for CK7,
    CK5/6, CAM-5.2 and AE1/AE3, but do not express S100,
    high-MW keratins and HMB-45, which helps differentiate from
    melanoma.
   Mastectomy or breast-conserving surgery involving removal of
    entire nipple-areolar complex followed by RTx. SLNB and/or
    AND if invasive disease or undergoing mastectomy (+ve LN in
    2/3rds with palpable mass). Adjuvant therapy is based on the
    stage of the disease.
   NB: Differential: chronic eczema, benign papilloma of the
    nipple, BCC, malignant melanoma, Bowen's disease.
   Paget's disease of the nipple. “an eczematous change in the skin of
    the nipple”. More than 95% of women with Paget's disease of the
    nipple have an underlying malignancy (90% invasive, 10% DCIS),
    although almost half are clinically and mammographically
    undetectable. Comprises 5% breast malignancies.
   Aetiology: 2 hypotheses. The in-situ transformation hypothesis
    suggests Paget's cells arise from transformed malignant keratinocytes
    and is thus a type of in-situ Ca of the skin. Consistent with this is the
    Paget's cells and underlying cancer are often separated by some
    distance. The epidermotropic hypothesis suggests ductal cells migrate
    along the basement membrane of ducts into the nipple epidermis.
    Immunohistochemical studies support this with similar staining of
    Paget's cells and the underlying carcinoma.
   Clinical presentation: burning, itching, change in sensation of nipple
    and areola are first symptoms. Skin lesion which is raised, irregular,
    and sharply demarcated from surrounding skin. May have erythema
    and scaling of nipple. Begins on nipple. Nipple retraction and
    discharge is not common.
1. Diagnosis
2. Definition
3. How is it treated?
   Inflammatory breast carcinoma
   A clinico-pathological entity with rapidly progressive,
    aggressive breast inflammatory process with erythema,
    oedema and warmth in overlying skin. Suspect if “infection”
    does not settle rapidly with 1-2 weeks of antibiotics. NB: often
    no distinct mass as tumour infiltrates breast diffusely.
    Inflammatory breast cancer is defined histologically by the
    presence of cancer cells in the sub-dermal lymphatics on skin
    biopsy.
   Triple assessment - Examination, MAMMO, USS and tissue
    diagnosis (skin biopsy and targeted core biopsy with hormone
    receptivity). Biopsy shows infiltrating carcinoma with invasion
    of subdermal lymphatics. METS tend to occur early and
    widely, and hence disease is rarely curable. Stage disease
    with CT CHEST/ABDO and bone scan. Discuss in Breast
    MDT. Aggressive neo-adjuvant hormone therapy, chemo- and
    radiotherapy.
Barium meal showing
extraluminal compression of
D2/D3. History of obstructive
jaundice, weight loss and back
pain in old man.

1. Most likely diagnosis?
2. Clinical findings?
3. Treatment options for the
diagnosis you have given.
   Head of pancreas tumour (probably adenocarcinoma). Double
    duct obstruction – obstructive jaundice, pancreatitic duct dilatation. Approx 1 in
    100 lifetime risk for pancreatic cancer.

   Steatorrhoea and weight loss, pain from pancreatitis or tumour
    infiltration of pain fibres, ask regarding late-onset diabetes
    without antecedent risks. Thrombophlebitis migrans. Stigmata
    weight loss. Jaundice. Anaemia. Virchow's node.
    Hepatomegaly or METS.Palpable gallbladder in painless
    jaundice (Courvoisier syndrome). Palpable mass. Succussion
    splash. Ascites. Sister Mary Joseph nodule and Blummer's
    shelf. [Measure glycoprotein carbohydrate tumour marker CA19-9, and if
    >200U/mL have 90% sensitivity, >1000 have high specificity (but also
    irresectability). Contrast-enhanced, tri-phasic MDCT scan of pancreas forms
    mainstay of diagnosis].

   Treatment options: defined by stage of disease and
    comorbidities. >80% present with irresectable disease;
    prognosis is poor even with surgical resection (median survival
    11-18mths, 10% 5yr survival). Medical/Radiation ONCO
    treatments some effectiveness in improving survival slightly.
   Palliative surgical options:
        Duodenal obstruction:
             Endoscopic stent or PEG/PEJ insertion
             Operative gastrojejunostomy (laparoscopic or open)‫‏‬
        Obstructive jaundice (N+V, intractable pruritus, progressive
         malnutrition):
             Endoscopic biliary stent via ERCP (plastic short-term, metallic
              longer durability)‫‏‬
             Radiological biliary stent
             Operative (choledocho-duodenostomy, choledocho-jejunostomy,
              cholecysto-jejunostomy, hepatico-jejunostomy)‫‏‬
        Pain:
             Analgesics, neuroleptics
             Laparoscopic Bilateral Transthoracic Splanchnicectomy
        Terminal palliation
A healthy 84-year-old woman
with a 6-month history of a
slowly growing asymptomatic
lesion on the dorsum of her right
hand.

1. Diagnosis
2. Pathology
3. Natural history
4. Treatment
   Keratotic cutaneous horn of invasive cutaneous SCC.
    Differential includes: other tumours, viral warts, actinic keratosis,
    keratoacanthoma, Bowen’s disease, seborrheic keratosis, and
    basal-cell carcinoma, sebaceous horn from ruptured sebaceous cyst
   MACRO: firm, erythematous, keratotic, plaque with indiscrete
    margins typically on sun exposed regions of body. MICRO:
    neoplastic proliferation of atypical keratinocytes extending into
    the dermis, with large hyperchromatic and pleomorphic nuclei.
    Layers of keratinizing squamous cells may produce “horn
    pearls”.
   Natural history of SCC is quite variable. May present as slowly
    growing, locally invasive lesion without METS or as a rapidly
    growing, widely invasive tumour with early MET spread. In
    general, those arising from actinic keratoses are more common
    and of slow growing type, whereas those from Bowen's
    disease, erythroplasia of Queyrat, chronic radiation dermatitis,
    scars, and chronic ulcers tend to be more aggressive. Those
    arising from normal skin, lips, genitalia and anal region also
    tend to be aggressive.
   Treatment is operative with curative intent involving complete
    surgical excision aiming for 1cm margin. Probably require skin
    graft (full or split-thickness). Palpable nodal METS (<5%)
    removed via selective nodal resection according to draining
    lymph basin. Small lesions amongst actinic field defect may initially be treated
    with topical chemotherapeutic agents (eg 5-FU, imiquimod).
Imaging finding:

1. Most likely diagnosis
2. Differential diagnosis
3. Pathogenesis most likely
4. Treatment
   Gas within bladder representing a colovesical fistula secondary
    diverticular disease
   Colovesical fistula secondary malignancy (eg colonic
    carcinoma, bladder carcinoma), Crohn's disease, radiation
    bowel injury, penetrating trauma, foreign bodies and iatrogenic
    injuries. Gas from recent urological operation. UTI with gas
    forming organism.
   Colovesical fistula is most common type fistulous
    communication between bladder and GI tract. M:F ratio 3:1.
    Diverticulitis is most common cause occurring in 2-4% cases.
    Clinically: may be completely asymptomatic. Typically
    refractory urinary tract infection, may have pneumaturia and/or
    faecaluria. Episode of diverticulitis may have gone completely
    unnoticed. O/E: NAD or pelvic mass. Rigid sigmoidoscopy
    usually NAD. Flexible sigmoidoscopy may disclose colon Ca or
    inflammation at fistula site. Cystoscopy shows bullous oedema,
    but fistula usually not visible. CT shows bladder air in 90%. Ba
    enema, USS, and cystography may miss small fistulae.
   Require exclusion of carcinoma in all cases. Inability to exclude
    cancer may prompt earlier operation. Treat Crohn’s
    disease.         Resection sigmoid colon if fistula persists, but
    no need for emergency or urgent operation. May have
    spontaneous drainage of paracolic abscess via fistula to
    bladder and operation may not be necessary. In up to 50%
    fistula closes spontaneously.
                                                       At operation: if
    suspect/confirmed cancer do not separate bladder from colon,
    rather resect en-bloc. For diverticulitis blunt dissection of colon
    off bladder, sigmoid resection, primary anastomosis +/-
    defunctioning ileostomy. Bladder side of fistula is sutured and
    the bladder is decompressed with a Foley catheter for 7-
    10days.
56yr female with previous
proctocolectomy.
1. Diagnosis
2. Natural history
3. Complications
4. Surveillance
   Primary sclerosing cholangitis
   Multiple intra- and extra-hepatic strictures in association with
    ulcerative colitis. Intermittent or progressive jaundice, with
    biliary disease sometimes pre-dating inflammatory bowel
    disease manifestation. Patients may also present with fatigue,
    pruritus, fever of unknown origin, or weight loss. Some patients
    present with the stigmata of chronic liver disease and cirrhosis.
    The onset and progression tend to be insidious.
   Recurrent obstructive jaundice and cholangitis, de novo biliary
    stone formation, cholangiocarcinoma (10-15%)‫‏‬
   Early detection of CCA is limited by a lack of reliable serologic,
    radiologic, and endoscopic findings. Biannual LFTs and CA 19-
    9. Annual MRCP. ERCP + brushings for malignant stricutres.
    Researchers at the Mayo Clinic have developed a multivariate statistical survival
    model from long-term survival data (Mayo risk score).The model computes the
    score on the basis of the patient's age, history of variceal bleeding, and serum
    levels of albumin, bilirubin, and aspartate aminotransferase.
              Q8
1. Describe findings
2. Diagnosis
3. Aetiology
4. How would you manage
this?
1. Diagnosis
2. Aetiology
3. How would you manage
this?
1. Diagnosis
2. Pathogenesis
3. Complications
4. Management
 What is the diagnosis?
 Name 3 causes for this
 lesion
 What are potential
 complications of this
 lesion?
 List the Forrest criteria
 Discuss its virulence
 factors
 Name diagnostic tests for
 this organism
 Name this organism
 What is your treatment?
 What is the diagnosis?
 Name associated
 conditions with this
 diagnosis
 What are the
 histopathological features
 What is your treatment?
 What is the diagnosis?
 Discuss this condition
 What is your
 management?
 Diagnosis
 List techniques for
 endoscopic control of UGI
 haemorrhage
 Factors predicting rebleed
 What is the diagnosis?
 Discuss the pathogenesis
 of this condition
 Describe the clinical
 presentation of this
 condition
Intra-operative finding:

1. Diagnosis
2. Aetiology
3. How would you manage
this?
1. Describe findings
2. Diagnosis
3. Aetiology
4. How would you manage
this?
   Left pupil smaller than right (miosis), left palpebral fissure
    narrower than right as the left upper eyelid is drooping
    (ptosis). Other likely features: anhidrosis, enopthalmus.
   Horner's syndrome
   A group of signs, usually unilateral, produced by paralysis of
    the cervical sympathetics whether of peripheral or central
    origin.
   Manage according to underlying cause. Neurologic or neuro-
    ophthalmic consultation may be considered. Interventional
    radiologic consultation in cases of suspected carotid artery
    dissection. Neurosurgical consultation should be considered
    in cases of suspected aneurysm. Surgical or oncologic
    consultation is dependent upon the particular etiology.
   MIOSIS: Appears at once after sympathectomy or block. Difference in
    size of pupils evident in daylight and accentuated in dim light since
    pupil does not dilate in dark. Yet pupil contracts briskly to light and
    convergence since third cranial nerve (thru ciliary ganglion) still
    controls sphincter pupillae. Homatropine but not cocaine dilates
    Horner pupil. Cilio-spinal pupil reflex lost.
   PTOSIS / NARROWING PALPEBRAL FISSURE: Due to combination
    of drooping of the upper lid and raising of the lower lid (at times with
    convex up appearance). Lid droops due to paralysis of non-striated
    part of levator palpebrae. Since voluntary portion of levator is
    controlled by 3rd nerve, ptosed lid can be voluntarily raised. Hence
    ptosis of Horner's syndrome is a pseudo-ptosis.
   ENOPHTALMOS: This is usually due to an optical illusion produced
    by the narrowed palpebral fissure. Evidence favors idea that muscle
    of Muller although important in animals is vestigial in man and does
    not contribute to either enophthalmos by paralysis or exophthalmas by
    stimulation. Occasionally atrophy of orbit contents and hypotony of
    globe produce some degree of enophthalmos
   ANHIDROSIS: Lack of sweating on ipsilateral side.
   First-order neuron lesions: Arnold-Chiari malformation, Basal
    meningitis (eg, syphilis), Basal skull tumors, Cerebral vascular
    accident (CVA)/Wallenberg syndrome (lateral medullary syndrome),
    Demyelinating disease (eg, multiple sclerosis, Intrapontine
    hemorrhage, Neck trauma (eg, traumatic dislocation of cervical
    vertebrae, traumatic dissection of the vertebral artery), Pituitary tumor,
    Syringomyelia
   Second-order neuron lesions: Pancoast tumor (tumor in the apex of
    the lung - most commonly squamous cell carcinoma), Birth trauma
    with injury to lower brachial plexus, Cervical rib, Aneurysm/dissection
    of aorta, Subclavian or CCA, Central venous catheterization,
    Trauma/surgical injury (eg, radical neck dissection, thyroidectomy,
    carotid angiography, coronary artery bypass graft), Chest tubes,
    Lymphadenopathy (eg, Hodgkin disease, leukemia, tuberculosis,
    mediastinal tumors), Mandibular tooth abscess, Lesions of the middle
    ear (eg, acute otitis media), Neuroblastoma
   Third-order neuron lesions: Internal carotid artery dissection, Raeder
    syndrome (paratrigeminal syndrome), Carotid cavernous fistula,
    Cluster/migraine headaches, Herpes zoster
1. Diagnosis
2. Aetiology
3. How would you manage
this?
   Rapidly growing Merkel Cell Carcinoma of the face in an elderly
    man.
   Merkel cell carcinoma (MCC), or neuroendocrine carcinoma of
    the skin, is an uncommon and often aggressive malignancy
    that has a poor prognosis. The Merkel cell is located in or near
    the basal layer of the epidermis and is closely associated with
    terminal axons. MCC is predominantly a tumor of the elderly,
    and most reported cases have occurred in Caucasians. It
    occurs most frequently in the head and neck region and in the
    extremities, and has a predilection for the periocular region.
    Risk factors are sun exposure and immunosuppression.
   Wide local excision or MOHS micrographic surgery, sentinel
    LNBx +/- ND, post-op RTx (plus CTx for Stage II). CTx alone
    for Stage III disease.
1. Diagnosis
2. Pathogenesis
3. Complications
4. Management
   Neurofibromatosis type I, with Lisch nodules (hamartomas of
    iris or freckling in the iris) and neurofibroma on the skin
   Autosomal dominant NF-1 gene on 17q codes for a protein
    called neurofibromin (tumor suppressor). 50% familial/50%
    sporadic.
   Neurofibromatosis alters or weakens this protein with rapid,
    radical growth of cells all over the body, especially around the
    nervous system. This leads to several tumors (optic glioma,
    neurofibromas and schwannomas). Lesions along visual,
    auditory, or CNS nerve pathways may result in blindness,
    deafness, or neurologic deficits. Also get high incidence of
    learning disabilities, increased chances of developing petit mal
    epilepsy (a Partial absence seizure disorder) and orthopeadic
    manifestations. Rarely renal artery stenosis and
    phaeochromocytoma.
   No cure exists for NF1 or NF2. The recommendations for
    follow-up include referral to support groups, psychological
    counselling, and evaluation for learning disorders; potential
    surgical excision of the lesions; and regular monitoring by a
    primary care provider for any lesion changes (patients with NF1
    are at a somewhat increased risk for malignancy). Audiologic
    examination performed before child is of school age. Annual
    ocular examinations are recommended. Genetic testing is also
    available for patients with NF who wish to have children.
    Historically, surgery has been a successful treatment for the
    lesions themselves; however, there is often recurrence, and
    nerve damage is a risk in cases in which the lesions are
    located along neural pathways
   A patient meeting two or more of the following criteria can be
    diagnosed as suffering from NF 1
           Neurofibromas - Two or more, or one plexiform
            neurofibroma
           Café-au-lait macules - Six or more measuring 1.5 cm in
            their greatest dimension
           Freckling - In the axillary or inguinal areas
           Optic glioma
           Iris hamartomas (Lisch nodules) - Two or more
           Sphenoid dysplasia or thinning of the cortex of the long
            bones
           First-degree relative
   What is the diagnosis?
   Name 3 causes for this
    lesion
   What are potential
    complications of this
    lesion?
   List the Forrest criteria
   Pre-pyloric ulceration (probably benign)‫‏‬
   H. pylori infection, NSAIDS, stress ulceration, combination of
    these
   Bleed, Block, Burst, Burrow, Become malignant (NB: H pylori
    infection (in childhood?) → atrophic gastritis → decreased
    gastric acid output → gastric cancer & decreased risk duodenal
    ulcer. Conversely H pylori associated DU lowers risk of gastric
    cancer by ? mechanism)
   Grade I: Active bleeding – Ia = spurting; Ib = oozing
    Grade 2: Ulcer with signif bleeding risk – IIa = non-bleeding
    visible vessel, IIb = adherent clot, IIc = red or dark blue flat spot
    Grade 3: ulcer with clean base
   Re-bleeding risks: Grade I 4-20%, Grade IIa ~10%, Grade IIb
    0-10%, Grade IIc 0-5%, Grade III 0-5%. Grade I and IIa
    mandate endoscopic therapy, IIb at endoscopists discretion.
   Name this organism
   Discuss its virulence factors
   Name diagnostic tests for
    this organism
   What is your treatment?
   Helicobacter pylori (non-sporing, G -ve curvilinear rod)‫‏‬
   cagA gene which codes cag pathogenicity island, vacA gene
    which codes for a vacuolating cytotoxin, bacterial
    lipopolysaccharide (endotoxin) and other proinflammatory
    proteins, urease enzyme which turns urea → ammonia thus
    buffering acid, flagella to allow movement into mucoid lining of
    stomach, adhesions to allow binding to epithelial cells (?
    especially cells that bear blood group O antigen)
   Rapid urease (sens 90%, spec 90-95%), serology (98, 100),
    culture (80, 100), microscopy (90, 90), carbon breath test [C13
    stable, C14 need gamma camera] (95, 95), faecal antigen (93,
    93), PCR on biopsies (>95 both)
   Klacid HP7: Amoxycillin 1.0g PO BD 1/52, Clarithromycin
    500mg PO BD 1/52, Omeprazole 20mg PO BD 2/52
   What is the diagnosis?
   Name associated
    conditions with this
    diagnosis
   What are the
    histopathological features
   What is your treatment?
   “Watermelon stomach” ie Gastric Antral Vascular Ectasia
   Chronic renal failure, collagen vascular disease, autoimmune
    connective tissue disorders, scleroderma, bone marrow
    transplantation, hereditary haemorrhagic telangiectasias, portal
    hypertension/liver cirrhosis
   Histologic hallmark is superficial fibromuscular hyperplasia of
    gastric antral mucosa with capillary ectasia and microvascular
    thrombosis in the lamina propria
   Argon plasma coagulation or Nd:YAG laser. Tranexamic acid,
    thalidomide, oestrogen + progesterone have been tried.
    Surgical antrectomy for unresponsive severe cases.
   What is the diagnosis?
   Discuss this condition
   What is your management?
   Dieulafoy's lesion (Exculceratio simplex)‫‏‬
   An abnormal tortuous artery that courses through the
    submucosal layer in the absence of an associated ulcer. 95%
    occur in the upper stomach within 6cm of GO junction
    commonly on the lesser curvature, however they can occur
    anywhere in the GI tract (duodenum 18%, colon 10%, jejunum
    2%, oesophagus 2%)‫‏‬
   Endoclip application and electrocautery
   Diagnosis
   List techniques for
    endoscopic control of UGI
    haemorrhage
   Forrest Grade 1b duodenal ulcer
   Injection therapy 1:10 000 Adrenaline (direct effect –
    vasoconstriction, platelet activation + subsequent stimulation of
    coagulation cascade; tamponade effect)
    Thermal: contact – heater probe, bipolar probe; non-contact –
    Nd:YAG laser, Argon plasma coagulation
    Mechanical devices: clips, loops, bands
    Combination therapy of above
   Rockall scoring predictors: SCRhAPS – Source of bleed, Co-
    morbid illnesses, Recent haemorrhage stigmata, Age,
    Presence of Shock. PEPTIC: failure to use Proton pump
    inhibitor post-procedure, Endoscopically demonstrated
    bleeding, Peptic ulcer as the source of bleed, Treatment with
    epinephrine monotherapy, Intravenous or LMW heparin use
    post-procedure, and moderate or severe Cirrhosis.
   What is the diagnosis?
   Discuss the pathogenesis
    of this condition
   Describe the clinical
    presentation of this
    condition
   Mallory-Weiss tear at gastro-oesophageal junction
   Sudden large transient pressure gradient across region of GO
    junction with acute distension of non-distensible lower
    oesophagus and relatively immobile lesser curvature of the
    gastric cardia. Another mechanism is violent prolapse or
    intussusception of upper stomach into the oesophagus.
   Retching or vomiting followed by haemetemesis reported in 30-
    85%. NB up to 50% have haemetemesis on 1st vomit, 85% total
    have haemetemesis, excess alcohol in 40-75%, aspirin in up to
    30%.
Intra-operative finding:

1. Diagnosis
2. Aetiology
3. How would you manage
this?
   Small bowel intussusception
   Invagination (or telescoping) of one loop of bowel into another.
    Rarely encountered in adults and usually caused by a benign
    or malignant polyp, intraluminal lesion or Meckel's diverticulum.
    More often seen in children; an organic lesionis not required,
    and the syndrome of colicky pain, passage of blood per rectum,
    and a palpable mass ( the intussuscepted segment) is
    characterisitic.
   Adult: Reduce the intussusception as far as possible, then
    resect affected bowel segment with end-to-end anastomosis
    (hand sewn).
    Child: squeeze intussusceptum back along the intussuscipiens.
    Ensure complete reduction. Only resect bowel if gangrenous
    bowel or unable to reduce, and I would then perform end-to-
    end anastomosis (hand sewn).

				
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