Gastro Mbchb4


Patterns of Pain
• SB → distension causes mid-abdo cramping
• LB → distension causes lower abdo cramping
• Duodenal → acid on ulcerated mucosa = epigastric burning pain
• Oesophagus → sens to acid (w or w/o ulceration) → retrosternal +/- epigastric
• Biliary tract → acute distension = RUQ pain (radiation to back)
• Ureters → acute distension = Loin pain (radiation to groin)
• Peritoneal inflammation → localised pain (felt at skin overlying inflammation)
• Bowel ischemia → severe generalised pain +/- peritoneal pain
• Referred pain (from spine)

Acute Abdo Pain

1. Types of Pain
• Don’t accept words like colic/cramps/sharp/stabbing/burning – w/o further explanation
• Biliary/renal colic – terms that refer to pain arising from these structures but does not imply pain of varying intensity (pain can often be severe + constant in both)
• Pain of varying intensity (waves); periodic (eg ev 5 or 10 mins) suggestive of bowel distension (particular from bowel obstr)
2. Onset and Progression
• Sudden onset of severe pain suggests viscus rupture, dissecting aneurysm or biliary/renal colic
• Progr of sev hrs more typical of inflame process – pancreatitis, cholecystitis, appendicitis
• No definite onset – lower chance of serious pathology
3. Duration (examples)
• Uncomplicated biliary colic only lasts a few hrs – 4-8h
• Pain that usu only lasts for a few hrs cannot be acute pancreatitis
• Pain that has been present for several weeks is not acute appendicitis
• Diverticular spasm lasts for hrs and is intermittent; pain from diverticulitis is in the same region but more severe/persistent and lasts for sev days or up to 2-3 wks + there will also be an element of peritoneal type pain
4. Alleviating factors
• Abdo contents are dynamic – subj to change
• Ask about rship to meals, bowel motions (passing flatus), swallowing, relief by not eating/aggrav by meals, effect of postural change, passing urine, menst cycle, assoc w vomiting, aggrav by deep breathing
• Clues to peritoneal irritation (not over peritonitis) – pain aggravated by coughing, straining, sudden mvment (eg car bumps)
• Patterns of subacute SB obstr – peri-umbilical cramping pain 30-60 mins after meals; assoc sxs incl vomiting (feculent), nausea
• LBO – vomiting (late), mainly obstipation, incr abdo distension

• General – vital signs, expressions of pain, restlessness or extremely still
• Abdo – tenderness and guarding, presence/absence of bowel sounds, tender abdo mass (diverticular or appendiceal abscess / inflammatory mass in IBD), rectal/pelvic exam (as appropriate)
• Others – jaundice, chest exmn

Chronic Abdo Pain

a. Chronic intermittent
• Frequent – up to daily
• Dyspepsia/reflux – upper abdo/retrostenral, related to meals
• DU – epigastric, worse on empty stomach
• IBS – pain anywhere in abdo but usu lower abdo, some assoc w variable bowel habit
• Diverticular dis – LLQ, relieved by passing flatus or b/m
• Constipation – lower abdo cramping, generalised distension, bloating
• MS – mus strain, referred from thoracic spine, n entrapment
• Inflammatory dis of colon – pain more common with crohns dis, pain can be due to peritoneal irritation or subacute obstr
• Pelvic pain – endometriosis, ovarian path, tubal sepsis (PID)
• Less frequent – discrete episodes
• Biliary colic – discrete episodes of RUQ pain lasting 2-8 h
• Renal colic

b. Chronic unrelenting
• Abdo malignancy – esp pancreatic ca or liver mets
• Thoracic spine – referred pain from fracture or mets
• Chronic pancreatitis (rare)

Chronic Intractable Pain (>6 months, no identifiable cause)
a. Feats of the pain
• Does not vary in intensity or character – no alleviating/aggravating factors
• Description is dramatic
• Triggered (+ maintained) by stressful life events
• Multiple other somatic complaints
• Major effect on family/social/work activities
• Multiple txs have been tried and failed – many adverse reactions
• Often assoc w depr, anxiety and pre-occupation w pain
• Illness beh – avoidance of family/personal/work tensions, 2ndry gain, pain-prone personality, low self-esteem, traumatic c/hood
b. Approach to mgt
• Make a realistic closure to ixs
• Accept the pain description – don’t get into organic/psychological debate, acknowledge the uncertainty
• Emphasise the absence of nasty pathology
• Emphasise they are not alone, it is common to reach this dx w chr abdo pain
• Focus on coping with the pain and improved function rather than cure
• Explore chr pain txs – TCAs, SSRIs, pain clinics (relaxation training, biofeedback, hyponosis, psychotherapy)
• Remain supportive and offer further (and frequent) review


• Change in consistency; semi-formed; watery
• Freq >3 / day
• Vol / weight > 200g / day

• Occupation, living conditions, sources of drinking water
• Previous gastroenteritis
• Unusual diets, change in diet, potential foods that aggravate diarrhea (coffee, soft diets, fruit juices, artificial sweatners)
• High vol watery stool – no reduction w fasting → secretory diarrhea
• Blood/mucus → IBD
• Weight loss
• Fatty stool → malabsorption
• Past hx – radiation, surgery, malignancy
• Family hx – celiac dis, IBD, polyps, bowel ca
• Meds – alcohol, freq A/Bs, fluoxetine, colchicines, metformin

• Clinical signs of malabsorption – mouth ulcers (celiac dis, IBD)
• Abdo tenderness – Crohns
• Abdo masses – malignancy
• DRE / Sigmoidoscopy

• Fecal specs – wbcs, rbcs, microscopy, culture, EIA for giardia antigen
• Bloods – FBC, ESR, LFT, Fe studies, folate/B12, TFT, endomysial antibody and transglutaminase antibody for celiac dis
• Gastroscopy/Colonoscopy incl distal duodenal biopsy and ileoscopy → random biopsies of ileum and colon
If dx still unclear; consider –
• More tests for malabsorption – 3 day fecal fat, vit A/D, INR
• Check urine for laxatives, pancreatic tests, gut hormones, autonomic function tests, stool osmotic gap
• Empiric trials – low lactose diet, metronidazole, cholestryamine

Maldigestion Impaired nutrient hydrolysis (intra-luminal)
Malabsorption Defective mucosal absorption of nutrients (clinical malabsorption covers all aspects of defective digestion/absorption

Conditions causing malabsorption

1. Celiac disease
2. Microscopic colitis
3. Tropical sprue
4. Bacterial overgrowth in SB
5. SB resection

1. Celiac Disease
Epidem Most common cause malabsorption
Predominantly european (1/100)
Strong assoc w HLA-DQ2/8 – 8% of first degree relatives have celiac dis (some asx)
Pathogen Gluten exposure reqd → abnormal cellular + humeral response to gliadin (component of gluten) → mucosal damage
Expos of immunologically active epitope requires tis transglutaminase (an extracellular matrix enzyme)
Path Villous atrophy + Crypt hypertrophy + intraepithelial lymphocytes
Pathophys Loss of brush border enzymes, loss of stimulus for pancreatic + bile secretion, exudation of protein across denuded mucosa
Pres Childhood
• Diarrhea, irritable, poor appetite
• May present as Fe deficiency, short stature, abdo distension, finger clubbing
• Relatively asx – mild bloating, abdo discomfort, incr wind (incr dx of mild cases w use of targeted screening w antibody tests)
• Anemia – unexplained Fe or folate deficiency
• Weight loss usual
• Diarrhea (constipation possible), abdo discomfort, borborygmi (rumbling/gurgling noises produced by mvment of gas/fluid or both in gut, audible at distance)
• Specific nutritional deficiencies – bruising, tingling (low calcium)
• Assoc w hyposplenism, dermatitis herpatiformis
Ixs Endomysial Antibody and tissue transglutaminase – 95% accurate
Dx confirmed by gastroscopy and distal duodenal biopsy
Tx 1. Gluten free diet – avoid products made from wheat, rye an barley (oats may be ok)
2. Specific dietary supplements (initially) – Fe, Folate, Vit D
Repeat duodenal biopsy rarely reqd, response monitored by a fall in tis transglutaminase antibody + improvement in nutritional indices
Complics Intestinal lymphoma (minimal risk if gluten free diet)
Osteoporosis – bone mineral density check reqd (if dx >40 y)

2. Microscopic colitis
• Triad 1. watery diarrhea, 2. normal colonoscopy, 3. microscopic colitis of unknown cause
• Two main types – 1. collagenous colitis, 2. lymphocytic colitis
• More common in elderly
• Tx empiric – loperamide, 5-ASA, steroids, cholestryamine, bismuth, metronidazole all have modest success rates
• Usu resolves after several yrs

3. Tropical Sprue (post-infective tropical malabsorption)
• Most commonly from travel SE Asia
• Path – subtotal villous atrophy
• Clin – persisting diarrhea + macrocytic anemia (usu low serum folate +/- low albumin)
• Tx – tetracycline 250 mg qid + folic acid 5 mg for 1-2 months

4. Bacterial overgrowth in SB
• ↑ conc of bacteria in jejunum
• Predisposing factors
 ↓ gastric acid secr
 ↓ SB motility
 Hypogammaglobulinaemia
 Structural – blind loop, jejunal diverticulae, SB stricture, enterocolic fistula
 Infiltrative dis – amyloid
 Vascular dis – scleroderma, SLE
• Effects – bile salt deconjugation, mucosal damage
• Pres – diarrhea, weight loss, megaloblastic anemia
• Dx – check fat soluble vits and B12, lactulose (hydrogen breath test may help)
• Tx – usu given empiric antibiotics (tetracycline, metronidazole, ciprofloxacin)

5. SB Resection
• Ileal resection – 50-100cm may cause diarrhea
• Pres
 Diarrhea – ↑ colonic bile acid concentrations stimulate Na + H20 secr → tx w cholestyramine and low fat diet
 Vit B12 deficiency – regular B12 injections
 Gallstones – due to ↓ bile acid pool
 Renal oxalate stones - ↑ calcium oxalate absorption
• Massive SB resection → careful nutritional support
 Avoidance of Na and H20 depletion
 Avoid hyperosmolar feds
 Avoid lactose
 Low fat diet
 ↓ gastric acid secr
 Antimotility drugs – loperamide
 Medium chain TGs
 Check for Mg2+ depl
 Promote calcium balance w Vit D + oral calcium
 Trace element deficiency, essential fatty acid deficiencies
• Some pts will require permenant TPN

Other causes of SB and LB disease

a. Radiation damage to gut
• A few pts w sig radiation exposure to gut → chr ischaemic changes (usu presents 2-5 y post exposure or up to 20 y later)
• Pres w partial bowel obstruction from strictures, bleeding, malabsorption, weight loss (↓ oral intake); usu relentless progr of dis
• Dx – by hx, barium studies +/- endoscopy
• Correct nutrional probs, consider surgery, high risk bec of anastomotic breakdown (proximal defunctioning stoma may be only option)

b. Ischaemic injury to gut
• Acute mesenteric ischemia
 Pres – abdo pain
 Dx – by hx, abdo CT, angiography, emergency laparotomy
 Tx – resection of infracted gut usu the only option
• Mesenteric venous thrombosis
 RFs – hypercoagulable states, pancreatitis, OCP
 Pres – subacute w abdo pain
 Dx – by CT
• Chronic mesenteric ischaemia
 Pres – abdo pain 1h after meals w weight loss
 Dx – duplex U/S or angiography
• Ischaemic colitis
 Pres – usu L sided acute abdo pain w tenderness +/- rectal bleeding
 Segmental submucosal hem + edema (splenic flexure/desc colon)


• Highest risk popns – European (Maori rate 1/2 of non-Maori)
• Incidence ↑ in NZ
• Lifetime risk in NZ – 1/20 by 75 y, M>F
• 2nd cause of ca death (M), 3rd (F)
• Wide variation betw countries – attributed to dietary factors (red meta intake, animal fat, dairy, low fruit/vege)
• RFs – low physical exercise, smoking, alcohol
• PFs – calcium, Vit D, folate, NSAIDs, aspirin

• >90% of CR ca arise from adenoma
• Found more freq in high risk popns – 25% of 55y olds have colonic polyps
• M>F
• May have fingerlike / villous structures (villous adenoma)
• Usu no sxs but may bleed → up to 5% become malignant (transition from adenoma→malignancy = 5-10 y)
• High risk adenomas = severe dysplasia, villous, >1cm

Hyperplastic polyps are not precancerous

Hereditary/Genetic Factors

1. Hereditary non-polyposis colorectal ca (HNPCC)
• 2-3% of all CRCs
• CRC risk ~75% by 70y
• Age of onset 40’s, R sided tumors predominate
• Assoc w extra-colonic tumors (endometrium, SB, ureter, renal pelvis)
• Modified Amsterdam criteria – clinical dx
i. 3 or more relatives w CRC or one of assoc tumors
ii. 2 or more affected individuals are 1st degree relatives
iii. CRC involve 2 or more generations
iv. 1 or more pts CRC cases dx <50 y
• Germline mutations in mismatch repair genes – 90% of mutations on chrom 2p or 3p (hMSH2, hMLH1 etc) → accum of unrepaired replication errors, detectable in tumor as microsatelite instability (pres in 90% of HNPCC tumors vs. 15% of CRC tumors)
• Loss of expr for proteins produced by mismatch repair genes can be detected in tumors by immunohistochemical tests
• Genetic testing avail
• Risk of CRC managed by surveillance colonoscopy – 2 early from 20-25y (adenoma→carcinoma seq may be accelerated)
• Sporadic CRC dx <50y should have tests for HNPCC, currently immunohistochemistry for loss of expr mismatch repair genes

2. Familial adenomatous polyposis (FAP)
• 0.5%-1% of CRC
• AD – mutation of APC gene
• Affected subjects develop 100s-1000s of adenomas
• Polyps develop soon after puberty, 1 or more cancers develop by age 40
• Genetic testing available – protein truncation test or sequencing
• Screening from 12-14y; 1-2 y sigmoidoscopy
• Ca prev achieved by prophylactic colectomy w ileorectal anastomosis initially or ileo-anal pouch
• Attenuated forms of FAP – multiple adenomas but may be <100; later age onset
• Extracolonic tumors – duodenal ca (~5%); gastroscopy screening after age 30

3. Peutz-Jeghers Syndrome + Others
• AD – assoc w circumoral pigmentation + hemartomatous polpys throughout GI tr
• Pts usu present w intestinal obstr due to intussuseption
• Prophylactic polypectomy may prevent future episodes and malignant transformation of polyps

4. Sporadic Bowel Cancer
• 20% of pts w CRC → FHx of CRC
• 1st degr relatives ~2x ↑ lifetime risk
• 2 x 1st degr relatives ~3x ↑ lifetime risk
• Younger age at dx of relative (<55y) ↑ risk >3x
• Pts w moderate risk (3x) should be offered 5y colonscopy starting 10 y earlier than index case
• Site of colon ca – 40% rectum, 30% sigmoid, 30% rest of colon
• Pathology – bowel cancers may be protuberant, ulcerating or structuring (majority are adenocarcinomas; ~10% secreting abudent mucin)
• Dukes Classification
• A – within wall, node neg 15% of cases 90% survival
• B – beyond wall, node neg 35% of cases 60% survival
• C – node pos 50% 30% survival
• Median survival w liver mets = 7 months

Clinical Aspects

1. Rectal bleeding (distal tumor)
2. Change in bowel habit (both diarrhea or constipation); rectal lesions may secr abundant clear mucus having appearance of diarrhea (also occurs w large rectal villous adenomas)
3. Iron deficiency anemia (esp R sided tumors)
4. Colicky lower abdo pain +/- distension (suggesting obstruction) – more common pres for L sided cancers
5. Abdo mass (usu in RIF)
20% are emergency admissions – usu obstr, occasionally perforation

• Sigmoidoscopy, then colonoscopy
• Colonscopy – igher sens for detecting colyps and allows for polypectomy at time of exmn
• Barium enema – may miss Ca of caecum if poor quality exam or sigmoid ca if severe diverticular dis

A. Colon Ca
• Primary tx – surgical
• Bowel prep, antibiotic prophylaxis, prev of DVT
• Resection of segment of involved colon incl associated mesentery and most prox L/Ns eg R hemicolectomy, R extended hemicolectomy, transverse colectomy, L hemicolectomy, sigmoid colectomy
• When resection deemed curative – no further Rx
• Dukes C pts – should be offered adjuvant chemo w 5-fluorouracil and levamisole
• Liver mets – some cases may benefit from segmental liver resection
B. Rectal Ca
• Assessment of stage, loco-regional spread, penetr fascia propria (MRI, endorectal U/S)
• Ant resection + total mesorectal excision (TME, aka EFE – extrafascial excision) + primary anastomosis is possible for majority where propria fascia not involved (2 cm distal margin of clearance is safe unless poorly differentiated)
• Ca of lower 1/3 rectum – sphincter perversion possible w colo-anal anastomosis and colon-anal pouch
• Abdomino-perineal resection may be reqd (~15%) due to sphincter involve - distal sigmoid, rectum and anus removed through combined abdo + perineal incisions
• Role of adjuv chemo in addition to mesorectal excision still under eval (may reduce local recur esp in v low tumors)
No evidence that routine F-up w CT/Colonscopy can improve survival
Local recur (desp TME w clear lateral margins) is difficult to tx + often a predictor of widespread dis
C. Malignant Polyps
• A focus of ca w pre-existing adenoma
• Removal by colonscopic polypectomy
• No further tx reqd if complete excision and no evidence of invasion of vasculature/lymphatics (if doubt → segmental resection)

Prevention CRC
A. Popn based / community change through educ
• Dietary change
• ↓ diary/animal fat intake
• High fiber sources – eg fruit/veg
• Chemoprevention
• Vit C/E, Folate
• Calcium
• Aspirin/NSAIDs
B. Clinical practice
• Targeting high risk grps – ie hereditary predisp (screening colonscopy for moderate/high risk individuals)
• Improved use of ixs – earlier dx leading to better Dukes stage
C. Popn screening of ave risk individuals
• Fecal occult blood tests
• Limitations – other causes of bleeding, not all tumors bleed
• ~15% ↓ CRC mortality
• For every 10 people w FOB +ve → 1 will detect ca, 3 will detect adenomas >10mm, 6 will be N
• Will cause incr demand for colonoscopy
• Flexible sigmoidoscopy – 70-70% of CRC accessible ?
• New fecal molecular tests for mutations may be developed – too expensive currently
• Screening colonoscopy – at 50y and 60y
• National polyp study showed 80-90% reduction rate in CRC after colonoscopic polypectomy
• Need participation rate of 44% to gain 35% reduction in CRC mortality
• Virtual colonoscopy
• Potential screening test – still may have limited acceptance bec bowel prep required and still requires air insufflation
• Not able to detect small polpys
• Approx 25% still need colonscopy to remove polpys


• Dietary
• Colonic slow transit – main cause of severe idiopathic constipation in adults
• Assoc w IBS and diverticular dis
• Drugs – opiates, CCBs, anticholinergics, phenothiazines, aluminium-containing antacids
• Depr, Anxiety
• Hypothyroidism
• Spinal cord disease
• Hirschsprung’s dis – segmental absence of myenteric nerves (usu dx in infancy, occasionally present in adults)

Key aspects of Mgt
• High fibre diet (may aggravate bloating)
• Fibre supplements - physillium seed (metamucil) or isphagula (normacol/isogel)
• Lactulose – good options, S.eff incl bloating or faeces leakage if overdone
• Stool softners – coloxyl unhelpful, used mainly for tx of painful anal conditions
• Stimulant laxatives (senna, bisacodyl) – theoretical risk of LT damage to myenteric plexus, however for many pts w slow-transit constipation, stimulant laxatives remain the only effective tx (usu prescribed as coloxyl with senna); safe LT dose up to 6 tabs/week
• Osmotic laxatives – Mg salts, colonscopy lavage solutions (now available as sachets – Movicol) are v effective, generally used for ST tx but can be used LT
• Kiwifruit concentrates are effective
• Need to predict and prevent probs – eg. a. starting chemo with vincristine, b. starting opiates, c. post-op, d. prolonged immobility
• Elderly – fecal retention can lead to fecal incontinence, intestinal obstr, urinary retention and restlessness; contributing factors are reduced mobility, impaired intellectual function, poor access to toilets, anticholinergic drugs, parkinsons

• Reqd if simple measures are not working
• Serum calcium, TFT
• Plain AXR – to assess degree of fecal loading (may have sig fecal loading, even if bowel habits seem reasonable)
• Barium enema (or colonscopy) to excl malignancy – unlikely if LT sxs and check for dilated colon (megacolon may be idiopathic or 2’ to hirshsprungs dis, LT psychotropic drugs, chr idiopathic pseudo-obstruction
• Colonic transit study can be useful – objective confirmation of prob; may help differentiate a generalised colonic motility prob (slow transit) from obstr defecation (rectal prolapse / rectocoele / defective ano-rectal co-ord)
• Specialist assessment – incl checking for rectal prolapse, rectocoele, competence of anal sphincters
• Further tests – defectating proctogram, transit studies, ano-rectal manometry

Layering of meds (like WHO pain ladder).
1. Diet → water ++, kiwifruit (laxative)
2. Metamucil
3. Lactulose 10-20 ml BD PRN
4. Coloxyl + senna (Laxol) one or two BD
5. Movicol sachets BD PRN


Dyspepsia Upper abdo discomfort >2 weeks
Some r/ship w meals helpful in linking w upper GI tr
Upper abdo discomfort usu arises from upper GI tr, but many pts w IBS have upper abdo discomfort
Acute/Severe sxs Consider alternative dx – eg myocardial ischemia, pancreatitis, biliary colic
Main causes a. Functional dyspepsia (most common, unknown pathophysiology) – see below
b. GOR – some pts complain of upper abdo discomfort, not heartburn
c. PU dis – ↓ incidence

Emperic tx usu given before ix - PPI/H2 antagonists often successful
Referral – influenced by gge of pt, degree of anxiety
Gastroscopy – accurate dx of reflux esophagitis, biopsy of suspicious lesions, H.pylori testing
Barium meal – only useful if dysphagia
Upper abdo U/S – reqd for more discrete and severe episodes of upper abdo pain → excl biliary colic (gallstones)
For more chr sxs such as bloating after fatty meals (dysmotility-type dyspepsia) will show gallstones in a proportion (~20% if >50y), but likely to be asx gallstones (common cause of persisting sxs after cholecystectomy)

Functional Dyspepsia
Normal gastroscopy, normal U/S, no response to PPI tx
Sxs – some sxs in some pts may be related to delayed gastric emptying
Mgt –
• Reassurance re absence of pathology
• Tx options limited
• Domperidone (motilium) may help post-prandial bloating, fullness, nausea
• Tx of H.pylori inf in absence of ulcer dis

Motilium (Domperidone)
• Dopamine antagonist with anti-emetic properties
• Anti-emetic effect may be due to combined peripheral (gastrokineetic) effects and antagonism of central Da receptors in the chemoreceptor trigger zone
• Human studies → incr lower esophageal pres, improve antroduodenal motlity, accelerate gastric emptying


Dysphagia Difficulty swallowing; usu described as food sticking, problem usu at level of perceived obstr may can be referred to suprasternal notch
Globus Lump in throat, common and persistent feeling unrelated to swallowing

Hx 1. Duration? <3/12 (malignancy). Long duration (motility)
2. Sxs occur w ev meal? Yes (structural), No (motility)
3. Sxs getting worse? Malignancy
4. Pain on swallowing? Infective esophagitis
5. Difficulty initiating swallowing (pharyngeal) or sticking after initial swallow (esophagus)
6. Choking or nasal regurg? Pharyngeal
7. Tablets a problem? Pharyngeal
8. Same for liquids or solids? Esophageal motility
9. What type of food eaten at moment?
10. Possible to return to meal after initial problem? Motility

A. Oropharyngeal dysphagia
Difficulty initiating swallowing
Causes Neuro - CVA, Parkinsons’s, MND
Local - Extrinsic compression, neoplastic
Motility - Hypertensive UES or incomplete relaxation UES, premature closure of UES (likely cause of a zenker diverticulum aka pharyngoesophageal)
Mgt 1. Videofluroscopy
2. SLT assessment → altering food consistency and bolus size, safe swallow techniques
3. Cricopharyngeal myotomy
4. Closure of zenkers diverticulum

B. Esophageal Dysphagia (food sticking)
a. Intermittent sxs, solids only
Ring of fibrous tis at gastro-esophageal junction (Schatzki’s ring) or mild peptic stricture +/- motility problem
Leads to food bolus or steakhouse syndr
Dx - by radiology or endoscopy
Mgt - dilatation v effective, try Glucagon IV 1mg initially
Eosinophilic esophagitis also causes food bolus obstr (dx by biopsy) – occurs mainly in children/young adults, assoc w hayfever/asthma, tx w swallowed
steroid inhalers
b. Intermittent sxs, solids and liquids
Motility d/o 1. Non-specific motility d/o (impaired esophageal peristalsis)
2. Esophageal spasm (may have CP)
3. Achalasia – absence of LOS relaxation + ↓/absent peristalsis (esophagus is dilated w retained food/saliva when severe
1. Non-specific motility d/o
Limited tx
2. Esophageal spasm
Nitrates or Calcium antagonists (sublingual or oral)
Reassurance that pain not cardiac and not life thr
3. Achalasia
Typical radiology – impaired peristalsis, dilated esophagus, smooth tapering at lower end w intermittent passage of narrow jet of barium
Manometry – most accurate and sensitive dx test
Tx – 1. Dilation to disrupt LOS (Endoscopic), 2. Cardiomyotomy (laparoscopic), 3. Injection of botulinum toxin into sphincter (~1 y effect)

C. Progressive Sxs
Dysphagia for solids first, then semi-solids then liquids
Urgent ix reqd – endoscopy preferred over barium swallow as direct vision and biopsies more accurate for malignancy
a. Peptic esophageal stricture – not all pts have hx of heartburn, tx w dilatations + maintenance PPIs
b. Esophageal carcinoma – usu older, weight loss, more progression of dysphagia, heavy alcohol/tobacco use

Pain on swallowing; may occur with peptic esophagitis
Most common w infective esophagitis (candida, herpetic) or med-induced ulcers (minocycline used for acne tx)

Differential Dx Approach

1. In the lumen
a. food bolus
b. foreign body (eg false teeth)
2. In the wall
a. Inflammatory stricture (eg GI reflux)
b. Achalasia (impaired esoph peristalsis – LOS fails to relax properly in response to swallowing) – usu primary achalasia (unknown cause)
c. Carcinoma
d. Scleroderma
3. Outside the wall
a. Gotire
b. Pharyngeal pouch
c. Mediastinal tumor (bronchial carcinoma, lymphadenopathy)
d. Enlarged LAtr (mitral stenosis)
e. Thoracic aortic aneurysm
4. Neuromuscular d/os
a. Bulbar palsy
b. Guillan-barre syndr
c. CVA
d. MND
e. Myasenthia gravis


Squamous cell carcinoma OR Adenocarcinoma (acid related)

• Highest incidence – China, Iran, Russia, Sth Africa
• M>F 3>1
• RFs – smoking, alcohol, ?local diet
• Adenocardinoma of the lower 1/3 – becoming more common in western countries (? Related to incr incidence of barretts esophagus); majority of tumors in nz
• Possibly due to increased weight gain which increases acid secr or from better nutrition/eradication of h.pylori which also incr acid secr
• Barretts can occur w/o sxs

Esophagus lined by squamous epithelium
• Adenocarcinoma may arise from upgrwoth of a ca arising in cardia of stomach OR
• The lower esophagus may be replaced by columnar epith (barretts esophagus = a pre-malignant change)

• Progressive dysphagia (presents late as advanced ca)
• Weight loss
• Coughing or Aspiration (due to tracheo-esophageal fistula); rare

• Radiology and endoscopy complimentary – both usu reqd, endoscopy (biopsies); radiology more anatomical detail
• Staging – CT +/- Endoscopic U/S

A. Surgery
• Only ~20% of pts suitable for resection – due to spread of tumor or other medical probs
• Spread determines prog, respectability rates, cure rates
• Marked tendency for direct intramural extension (prox>distal)
• Direct invasion into mediastinal structures
• Lymphatic involve
• Distant blood borne mets
• Resection for selected pts offers change of cure
• Tumors of lower 1/3 (ivor-lewis procedure) – approach may be transthoracic or trans-hiatal
• Tumors of mid-upp thirds require 3 stage procedure requiring laparotomy, thoractomy and cervical incision
• Results of esophageal resection
• Operative mortality 8-10% (easy to negate survival benefit of surgery)
• Survival figs depend on selection criteria for surgery
• Overall 10-20% 5y survival (mean = 16 months)
• Surgery + Chemo likely to improve 5y survival
B. Palliation of Dysphagia
Mean survival = 6 months
a. Endoscopic intubation
• Self expanding metal stent
• Probs – blockage, migration, tumor growth at upper and lower margins and ingrowth into stent
• Overall – good palliation w minimal morbidity
b. Radiotherapy (+/- combined w chemo)
• SCC more radiosensitive – uncommon type
• Some delay before some palliation achieved
• May heal with stricture which requires intubation w a stent
• More intensive chemo-radiotherpay regimens offers cure rates p to 20% (comparable to surgery)


• Common cause cancer death worldwide
• High risk popns – SE asia/Japan, Russia, Sth America
• M/PI – 2-4x more common
• Incidence falling in countries adopting western lifestyle (except Japan)
• M:F 2:1
• Mean age 69y

• Usu arises in context of chr gastritis (H.pylori main culprit)
• RR of gastric ca in H.pylori infected individuals (2-4x)
• Other RFs ?dietary – polycyclic hydrocarbons (smoked food), vit c deficiency (decr anti-oxidant activity), nitrates (drinking water), pickled food, high salt, no refrigeration, low fruit/veg
• Atrophy gastric mucosa → ↓ gastric acidity → bacterial overgrowth (bacteria may convert nitrates→nitrites→carcinogenic N-nitrosamines
• Other RFs – PA, prev gastric surgery
• Genetic factors – mutation E-cadherin gene (first found in extended Maori family w high rate gastric ca); probably impt in sporadic gastric ca also
• Migration studies – eg Japan→Hawaii – confirm importance of etal factors

Early Gastric Ca
• Ca limited to mucosa or submucosa (regardless of presence/absence of L/N mets)
• Double contrast barium meal + endoscopy
• 5y survival excellent – dx at this stage rare in western countries

a. Location
• Cardia – becoming the most common site
b. Gross Appearance
• Often ulcerated w a raise everted edge
• May cause diffuse infiltration producing a thickened shrunken stomach w no visible change to lining mucosa
c. Histology
• Adenocarcinoma (intestinal or diffuse (lauren classification)) 90%, other types incl lymphoma 5%
Intestinal Cancers (gland forming)
• Assoc w chr gastritis and intestinal metaplasia
• Occur in high risk areas for gastric ca
• More common in males and older pts
Diffuse gastric cancers
• Usu infiltrating
• M=F, younger pts
• Genetic factors may be more impt (E-cadherin mutation)
d. Spread of gastric ca
• Initially – direct spread through gastric wall
• Involve of regional L/Ns common at time of dx
• Spread to distant sites also occurs
• Transperitoneal spread – typically seen in diffuse cancers

• Pres – early satiety, weight loss, anorexia, vomiting (non-specific or late occurring → generally too late to consider resection)
• Exmn – epigastric mass, succession splash from pyloric obstr, evidence of mets, L supraclav l/ns

• Operative tx – few candidates eligible for aggressive therapy
• Distal gastric ca → subtotal gastrectomy
• Proximal gastric ca with invasion of lower esophagus → esophagogastrectomy, splenectomy + reconstruction by esophageal anastomosis to a Roux-en-Y segment of jejunum (+/- extensive lymphadenectomy / resection of omentum)
• Adjuvant tx – some benefit, ECF (epirubicon, cisplatin, 5-fluorouracil)
• Non-operative palliation – pain relief, dysphagia relief (self expanding metal stents can relieve gastric outlet obstr)


Immediately on presentation; while taking the hx/exmn –
• Establish venous access
• FBC, U/E, INR, Renal + Liver function, Blood for cross match

1. Describe the bleeding
• Haematemesis – a. description of vomitus (coffee ground vs dark or bright red blood) b. amount, c. freq, d. duration
• Melaena – black tarry motions
• Anemia implies subacute blood loss – tiredness, weakness, SOB on exertion
• PR bleeding
• Bright red or dark red
• Estimate amount (large vol of altered blood may be from massive upper GI bleeding)
• Most lower GI bleeding is slow and intermittent and does not require hosp adm
• Perianal dis most common cause of minor intermittent bright red PR bleeding – a. hemorrhoids b. anal fissure
2. Any history relevant to possible causes?
• Indigestion – reflux or ulcer type sxs
• Aspirin or NSAIDs
• ?liver dis (alcohol intake, previous abnormal LFTs); ?esophageal varices
• Hx of previous bleeding – upper or lower
• Forceful vomiting preceding haematemesis
• Change in bowel habit
• Abdo pian (LLQ suggestive of diverticular dis)
3. General Med Hx – cardiac, respiratory, renal dis etc

1. Vital Signs – pulse (tachycardia first sign blood loss), BP (postural and supine hypotension), pallor, sweating, poor peripheral circ, perfusion
2. Signs of chr liver dis
3. Assess CV and Resp systems - ?HF, ?CORD
4. Examine abdomen
• Tenderness, signs of peritonism
• Abdo mass (?gastric malignancy, colonic mass, hepatomegaly)
• PR – check for melaena or blood

• Hb - ↓ suggests chr or subacute bleeding, may be normal and still compatible with major blood loss as equilibration may take >8h
• MCV - ↓ chr blood loss (iron deficiency anemia), ↑ alcohol related
• Platelets - ↓ in chr liver dis, ↑ in subacute blood loss
• LFTs – low albumin = ?cirrhosis, elevated liver enzymes (non-specific but alerts to possible liver dis),
• Coagulation – incr prothrombin ratio = ?cirrhosis


Causes of Upper GI bleeding (Endoscopic findings)
• DU or GU – 50%
• Gastric erosions - 20%
• Oesophagitis – 5%
• Esophageal varices – 5%
• Mallory-weiss tear – 5% (common in young pts)
• Gastric ca

Rapid risk assessment prior to endoscopy
• Predicted mortality and predicted risk of re-bleeding in hospital will help assess appropriate timing of endoscopy, alert to possible need for Endoscopic intervention +/- surgery, to deliver appropriate level of intensive care to higher risk pts and give confidence for early d/c.
Scoring System
Variable 0 1 2 3
Age <60 60-69 >=80
Shock Sys >100, PR <100 Sys >100, PR >100 Sys <100
Co-morbidity None major HF, IHD, any major RF, LF, disseminated malignancy
Dx Mallory-weiss, no All other Malignancy GI tr
lesion, no SRH
Major SRH none, dark spot only Blood in GI tr, adherent clot, vis or spurting vessel
*SRH = Endoscopic stigmata of recent hemorrhage – ie blood in stomach, adherent clot, visible vessel, spurting veseel
Score Mortality (no re-bleed) Mortality (with rebleed) Action
0-2 Nil Nil Early d/c
3 5% 5-10% ward-in patient
4-6 5-10% 15-25% ICU or HDU if appropriate
7+ 10-35% 30-50%

Management Principles for High Risk Patients
• Cross match 4-6 units of whole blood
• Resuscitate
• NG tube not recommended (does allow ID of blood in stomach but no proven benefit)
• Surg team review
• Discuss endoscopy timing with endoscopist
• Close observ of BP/PR (minm every 30 mins) – immed reporting to med team if sys <100 or a fall of >20 mmHg
• Care in observation – risk of rebleeding
• IV Omeprazole 20 mg Q12H (benefit shown with high risk ulcers only)
• Start Octreotide if strong suspicion of varices
Bleeding Ulcer
• Endoscopy and injection sclerotherapy if large ulcer, visible vessel or active bleeding (inject 1:10,000 adrenaline)
• Endoscopic intervention reduces hospital stay, rebleeding, surgical intervention and blood transfusions and mortality
• Surgery for uncontrolled bleeding after 2 attempts at Endoscopic hemostasis
• Surgery should be limited to overview of ulcer to control bleeding

• Overall mortality 5-10% (death not usu from uncontrolled bleeding ie liver dis, multi-sys illness, malignancy)
• Bleeding varicies – 40% mortality (mortality predicted by severity of liver dis), mortality from lower GI bleeding rare

Background data on NSAIDs and GI Bleeding
• Point prev of GU or DU in NSAID users ~ 20%
• GU to DU ratio 2:1
• ↑ risk 4-5x
• Annual incidence of major complications for regular users of NSAIDs 1-2%
• No warning sxs in 60% admitted to hosp
Relative risks of GI bleeding
• Brufen ~2.5, Diclofenac ~4, Naproxen ~6, Indomethacin ~9, Piroxicam ~15, Low dose aspirin ~2.5
Risk factors for NSAID induced complications
• Age >75y
• F
• Past hx ulcer and ulcer type dyspepsia
• Anticoagulants
• Steroids
• Low-dose aspirin
COX2 Inhibitors
• ↓ risk of bleeding/perforation by ~50% cf most traditional NSAIDs
• ↑ risk MI + CV death


• Diverticular disease – 50%
• Unknown – 20%
• Neoplasm – 10%
• Angiodysplasia – 10% (mostly >75y)
• Colitis and miscellaneous – 10%

• Ix – colonoscopy (usu once bleeding settled when easier to prep bowel); early colonoscopy (while active bleeding) allows for accurate dx of bleeding from diverticular disease
• Surgery rarely reqd to control lower GI bleeding (resection reqd if colonic malignancy)
• Bleeding settles spontaneously after appropr resus + transfusion
• Massive colonic bleeding may need ix by angiography prior to surgery
• Risk of recurrent bleeding after first diverticular bleed ~30%
• Angiodysplasia of colon (usu cecum) can be treated with argon plasma coagulation at time of colonoscopy, R-hemicolectomy rarely reqd

Iron Deficiency Anemia – Ixs
• >200 ml blood reqd to cause melaena, <200 ml daily will not be noticed
• Normal iron loss through minor GI loss = 1 gm/day
• Ave iron absorption 1-2 mg/day
• Losses >5-10 mls/day usu reqd before iron definciency anemia develops
• Iron defiency anemia (shen no obvious cause of bld loss) requires evaluation of upper + lower GI tr (approx 60-90% will have impt GI lesions)
• Causes
• Reflux esophagitis / Gastroduodenal ulceration / Large hiatus hernia (longitudinal erosions in hernia) – 30-70%
• Tumors – carcinoma colon or large colonic polyps – 10%
• Other – CD/Colitis, vascular malformation, NSAID related lesions, long-distance running – 10%
• Most common cause worldside – Hookworm!

Diagnostic Approach
• Is anemia secondary to iron deficiency?
• Consider MCV, serum Fe, IBC, ferritin, presence of microcytes/hypochromia
• Typical pattern of Fe deficiency = low serum Fe but raised TIBC
• Low MCV and normal Fe studies = thalassaemia
• Are there any reasons for anemia of chr dis – renal impairment or chr inflammation → check ESR
• If likely to be iron deficiency consider also – dietary hx of iron (rare in nz), menorrhagia, haematuria (rare) or anemia present over many yrs (eg celiac dis as a cause of Fe malabsorption); duodenal biopsy routine part of ix
• Combined gastroscopy/colonoscopy is mandatory for iron deficiency anemia (unless clearly caused by menorrhagia)

Obscure Bleeding
• Unknown despite gastroscopy and colonoscopy
• May present as overt bleeding (blood observed PR) or unexplained (and recurrent) iron deficiency
• Possible Causes –
• SB lesions – vascular abnormalities, ulceration (NSAIDs, CD), tumors (GIST, adenomas)
• Meckels diverticulum
• Ixs
• Capsule endoscopy (pillcam) – best ix for SB, preferably before any other studies to be cost-effective
• Meckels scan (younger pt) requires gastric mucosa within diverticulum
• SB enteroscopy (as f-up to capsule endoscopy, for prox lesion)
• Double balloon enteroscopy – technique for complete visualisation and access to all of the SB


Heartburn Retrosternal burning discomfort
GE Reflux Abnormal exposure of esophagus to gastric contents (+/- sxs)
Reflux Esophagitis Ulceration and inflammation of lower esophagus 2’ to reflux
GO Reflux disease Includes all clinically relevant manifestations of reflux

Prev 35% >1/ month, 7% daily

1. Transient relaxation of LOS
Normal physiology, vagally mediated reflex post-prandial, allows gas to escape from stomach
Does not occur in supine position
Majority of reflux episodes occur during transient LOS relaxations (if LOS resting pressures normal)
2. Low mean LOS pressure
Reflux episodes occur with a. ↑ abdo pres, b. bending, c. supine, d. gastric distension
3. Hiatus hernia
LOS above diaphragm → less effective barrier
Assoc w reflux, larger hernia = more severe hernia
Defences to GORD LOS and diaphragmatic sphincter mechanism
Effective esophageal acid clearance (peristalsis)
Neutralising effect of saliva and esophageal mucosal secretions
Intact mucosal diffusion barrier

Sxs Typical Heartburn, Regurg, Waterbrash, Belching
Warning Dysphagia, Odynophagia (pain on swallowing), Anaemia, Weight loss
Atypical Non-cardiac CP, Asthma, Hoarseness, Sore throat

Ixs 1. Endoscopy
<50% w reflux sxs → normal endoscopy
Presence of reflux esophagitis diagnostic
2. Ambulatory 24h esophageal pH monitoring
May help resolve some diagnostic problems
Correlation of pain with esophageal acid exposure useful
Helpful in non-cardiac CP, other atypical sxs, pts w troublesome sxs but endoscopy neg

Dx Hx of heartburn + symptomatic response to tx (therapeutic trial of omeprazole 40mg OD + sx diary)

Patterns of Reflux Disease
1. Mild disease (Majority)
Normal LOS pressure, intact sphincter mechanism, generally normal peristaltic activity
Mostly upright reflux assoc w post-prandial transient LOS sphincter relaxations
Freq short-lived reflux episodes, rapid clearance
2. Severe or complicated disease
Assoc w hiatus hernia, low LOS pres
Free passage of refluxate when supine (esp lying on R side) – more supine/nocturnal reflux
?More likely to cause mucosal damage
Barretts esophagus – decr sens to acid (less heartburn)
3. Hypersensitive esophagus
Normal esophageal acid exposure (normal pH study)
Most reflux episodes are appreciated at pain (heartburn)
Some assoc w IBS
4. Functional heartburn
Sxs suggest reflux but normal pH study and no correlation of sxs w reflux episodes
Common cause of failure to respond to PPI
Pathophys unknown

1. Lifestyle Stop smoking, weight reduction, alternating timing and constitutions of meals
2. Antacids Limited acid-neutralising function (largely ineffective in controlled trials)
3. H2 Antagonists Effective for mild dis, best choice for PRN tx bec of rapid onset (cf PPI)
4. PPI More effective control of gastric acid secr over 24h, single morning dose usu sufficient, bd if reqd for sx control, best given prior to meals
Failure to respond (~30%) due to –
a. inadequate acid suppr (incr dose to PPI bd 30 mins prior to meals + H2 antag at bedtime)
b. hypersens esophagus – may require incr dose, addition of low dose TCA, explanation + reassurance
c. wrong dx – angina, achalasia, esophageal spasm, IBS, gallstones
d. functional heartburn – non-acid related sx but sounds like heartburn
5. Laparoscopic fundoplication +/- Cruroplasty
Option for pts w sxs well-controlled on maintenance PPI who do not wish LT medication
Approach if volume reflux or resp sxs and unresponsive to medical Rx
Consider refractory sxs (as above, failure to respond) – need pH study
Operation may aggravate bloating and flatulence, inability to belch
Dysphagia common initial 3-6 months, but resolves in majority
Outcome of surgery – 85% good, 1-3% unhappy/ambivalent, ~25% will continue PPI

Complications of LT GE Reflux
1. Barretts esophagus Squamous→columnar lined esophagus (pre-malignant condition due to LT acid expos)
↑ risk esophageal malignancy (adenocarcinoma)
Higher risk of ca w incr length of involvement, ulceration within barretts epithelium, dysplasia on biopsy
No dysplasia → f-up gastroscopy 4y; low grade dysplasia repeat at 6mth; high grade repeat at 3mth + still high grade → distal esophagectomy)

IBD – Crohns Disease and Ulcerative Colitis

• ↑ incidence of CD
• CD >common Nth Europeans, rare in developing countries
• Smoking - ↑ risk CD, ↓ risk UC
• Emerging in other countries as middle class popn grows (theory – less expos to enteric infections → less tolerance of imm sys)

• Genetic knockout animal models of colitis; IL2 deficiency → UC, IL10 deficiency → CD; support critical role of T cells + CKs
• Genetics – first degree relatives 30x ↑ risk (8% lifetime risk) – multi-gene d/o
• Dysregulated immune response to normal intestinal bacteria, NOD2 gene involve in CD (gene encodes for protein involve in innate response to bact)
• ? infectious agents unlikely
• Diet + psyc factors no proven role in relapses


• Large bowel only
• Begins in rectum, spreads prox in continuity
• Mucosa inflamed (reddened with granular surface)
• Long standing dis → loss of haustral pattern
• Macroscopic ulceration does not occur except during severe attacks
• Microscopic appearance
• Inflam confined mainly to mucosa
• During acute attacks – neutrophils infiltrate through crypt epith to form crypt abscesses
• Chr inflame cells ↑ (esp plasma cells)
• Crypts show loss of goblet cells
• Paneth cell metaplasia
• During resolution, crypts regenerate, but imperfect healing leads to irregular branching or atrophy of crypts

• Sxs – 1. Diarrhea* (often with blood), 2. Frequent b/m +/- tenesmus or urgency, 3. LLQ or rectal discomfort, 4. Fever, 5. Malaise, 6. Weight loss
• Characterised by remission + relapses
• Extent of dis at 1st pres – a. Total colitis 25%, b. L-sided colitis 50%, c. Proctitis 25% (feces may be formed, pt troubled by PR bleeding, tenesmus/urg)
• Prognosis – 90% go into remission after first episode but have relapsing course

• Bloods - ↑ ESR, ↑ platelets
• Plain AXR → dilation of colon may give indication of extent of dis
• Colonscopy → determine extent + severity of disease, serial biopsies

• Infective colitis – C.jejuni, Salmonella spp
• Colonic CD – distinction impt mainly when considering surg
• Pseudomembranous colitis – complication of broad spec a/bs, C.difficile
• Ischemic colitis – elderly pts with vascular dis, radiological appearance of thumb printing

Extra-intestinal Manifestations
• Arthritis – 20% large joint polyarthropathy (knees, ankles, elbows, wrists), tends to relapse + remit w colitis
• Skin lesions – erythema nodosum, pyoderma gangrenosum (rapidly enlarging ulcerating lesion), may precede bowel dis, apthous mouth ulceration
• Ocular lesions – uveitis (iritis or episcleritis)
• Liver and biliary dis – sclerosing cholangitis (progressive cholestasis, irregular stricturing of intra and extra hepatic bile ducts), cholangiocarcinoma risk
• CR malignancy – incr risk of malignancy in UC (pan-colitis) after 10y of dis, 30y risk + 10%, surveillance colonscopy looking for dysplasia

• Acute attack
• Rectal steroids and/or 5-ASA (5-aminosalicytic acid / mesalazine) foam/liquid enema/suppository
• Oral 5-ASA (mesalazine) – Pentasa, Asacol, Dipentum
• Moderate to severe attack
• Add oral steroids
• If no response – admit for IV hydrocortisone (100mg Q8H)
• Severe attack
• Def = >6 b/m per day, fever >37.5, ESR >30, albumin <30
• Watch for complications of severe dis – toxic dilatation (megacolon), perforation and bleeding
• IV hydrocortisone 3-5 days – if no response → oral/iv cyclosporine or proceed directly to colectomy
• 70% will achieve remission
• Failure of Rx → urgent colectomy
• Possible alternative → infliximab 1-2 infusions (monoclonal antibody to TNF)
• Maintenace of remssion
• Sulphasalazine 2g/day or mesalazine 2g daily – prevents relapse
• After 12 months, 70% relapsed on placebo, 20% on 5-ASA or sulphasalazine
• 5-ASA preps do not have the sulphur moiety present in sulphasalazine and have ↓ incidence of side effects (rash, GI sxs, headache)
• Immunosuppressive agents (azathioprine) - ↑ usage for maintenance tx (usu periods 5-10y), delayed onset action, indicated if requirement for freq/prolonged courses of Prednisone
• Surgery
• Colectomy = cure
• Options – a. ileostomy or ileo-anal anastomosis with ileal pouch (continuance maintained w 3-6 b/ms per day
• Ileorectal anastomosis rarely used – potential for carcinoma in rectal stump
• Pouchitis (30%) – leading to incr urgency + freq (aetiology unclear), some response to metronidazole or ciprofloxacin
• Some extra-intestinal manifestations may persist – skin, liver probs, axial arthritis


• May affect any part of GI tract
• Begins as aphthous ulcers within epith overlying lymphoid aggregates
• Later ulceration characteristically fissuring or deeply penetrating
• Mucosa betw the fissuring ulcers is edematous (cobblestone appearance)
• Typically discontinuous
• Perianal manifestations – presence of small non-caseating epitheloid granulomas

Clinical features
• Vareity of sxs (depending on area of bowel involved; mouth→anus)
• Ileum/cecum 40%, SB only 30%, colon only 25%
• Terminal ileum disease – pain + localised tenderness RIF
• Colonic – diarrhea with blood, cramping lower abdo pain
• Rectal involvement – urgency, incontinence, bleeding
• Perianal dis – abscesses and fistulae (pres w pain + d/c)

• Intestinal obstruction – usu subacute
• Fistulae – from bowel to bowel/bladder/vagina/anterior abdo wall
• Systemic feats – sim to UC
• Nutritional deficiencies
• Anemia – iron or folate deficiency, chronic dis, blood loss
• Hypoproteinemia – protein loss and malnutrition
• Malabsorption fat soluble vitamins, vit B, vit c, zine (less common)
• Osteoporosis – may relate to steroids, low dietary calcium, early mp

• Colonoscopy + ileoscopy
• SB enema
• CT scan (if suggested extra-colinic dis eg abscess or fistula)

• Colonic – UC
• Ileo-colinic – TB, Yersinia inf (acute terminal ileitis), appendix abscess, cacrcinoma of caecum, lymphoma
• Sigmoid – diverticular dis

Dietary - Nutritional deficiencies identified and treated, supplemental oral feeding with polymeric liquid, parenteral nutrition (surgical adjunct for complic dis)
Anti-inflammatory drugs
• Steroids – benefit in active dis, start 40mg OD ↓ w clinical improvement, ideally stopping 6-8w
• 5-ASA containing drugs – effective in active dis, mainly colonic dis, slow release formulations (pentasa) modest use in maintenance
• Immunosuppressives – azathioprine and methotrexate, v useful steroid sparing agents, aza most common tx (1/3 of pts w CD on aza at some stage)
• Antibiotics – surgical drainage reqd for intra-abdo pus but broad-spec cover also reqd, metronidazole + ciprofloxacin useful for ano-rectal dis
• Infliximab (anti-TNF monoclonal antibody) – effective tx for severe dis, 70% response, may achieve complete mucosal healing, ST response only 2-3m, maintenance tx effective but minimal use in nz due to cost
• Resection of diseased segment of bowel relieves sxs but does not cure dis
• Surgery indicated if a. failed medical tx, b. unacceptable s.effs from tx, c. complications (obstruction, intraperitoneal abscess, enteric fistulae, hem)
• Choice of operation – usu resection (conserve approach to resection margins to maintain as much functional bowel as possible); stricturoplasty conserves bowel and relieves obstr
• Need for surgery in ileocolitis ~45% at 7y, 80% at 15y
• Recurrence post-surg – sx recurrence 35-65% at 5y, Endoscopic recurrence early after ileal resection
• Azathioprine, high dose 5-ASA (Pentasa) + metronidazole all reduce recurrence rate after resection
• Only some pts benefit from prophylaxis – case selection difficult due to course of dis unpredictable
• Stopping smoking delays recurrence
• Colinic dis – more difficult surgical options, proctocolectomy and ileostomy vs segmental excision, need to balance benefit of avoiding ileostomy w potential for recurrent dis and need for further surgery, recurrence in rectum w ileo-rectal anastomosis high
• Anorectal dis – surgery to allow drainage, but radical excisions of fistulae may lead to complications, pre-op MRI impt for identying collections around sphincterse



• pt may describe diarrhea to mean incr bowel freq, but vol of bowel motions normal, main sx may be urgency
• alternating diarrhea/constipation is a key sx
• long hx of similar sxs (several years) gives much greater confidence that the dx is functional bowel dis
• post-infectious IBS is common (sxs may take up to 2 yrs to resolve)
• Abdo bloating is often part of IBS but can be the sole PC
Sxs not part of IBS
• Nocturnal diarrhea or nocturnal abdo pain, rectal bleeding, weight loss
• Rectal bleeding may be due to local causes (anal fissures or hemorrhoids) which can be aggravated by variable bowel habit
• Any pt w high stool vol (>200 mls / day) for >4 wks should be investigated further
• Stool consistency suggesting malabsorption – pale, greasy, offensive stool that floats and is difficult to flush
Non-GI sxs assoc w IBS (unknown reasons)
• Dysmenorrhea, dyspareunia, urinary freq, nocturia, sens of incomplete bladder emptying, fatigue, palpitations

IBS – background info
• Common – 15-20% prev across all ages, F>M (slightly)
• LT studies - 10% of subjects initially free of sxs had IBS after 1-2 y and same proportion lost their sxs over the same interval
• Pts who consult have higher levels of anxiety and ↑ prev psyc illness, but also have a higher severity of sxs

• Abnormal muscle/motor activity of SI and colon - altered transit times demonstrated in reaction to mental/physical stress
• Visceral hypersensitivity (partly abnormal awareness of normal physiology), heightened awareness of colonic distension

• FBC (ESR), LFT, Celiac antibodies, iron studies, folate/b12 deficiency
• Sigmoidoscopy
• Barium enema or Colonoscopy reqd for pts >40y
• Recent change in bowel habit (w/o obvious explanation) → colonoscopy

1. Explanation + Reassurance
• Sxs tend to persist on an intermittent basis
• Structural normality + absence of ids
• Discuss the problem in terms of overactive or oversensitive gut
2. Ixs sufficient to allay fears/anxieties re ca (colonoscopy esp helpful if ca fear main problem)
3. Therapeutics
• Fibre supplements – may help sxs of constip + incomplete evac; abdo pain not usu improved, may aggravate bloating; ltd efficacy
• Laxatives – if prominent constipation → kiwifruit, Mg2+ compounds, avoid lactulose
• Loperamide – for prominent diarrhea + urgency (1-2 caps / day) → v helpful if urgency combined w low anal tone and incontinence
• Anti-spasmodics – anti-cholinergics (eg mebeverine) are of modest benefit for painful abdo cramps, side effects limit usefulness
4. Dietary
• Exclusions
• Gas forming foods – esp wheat, some vegetables (eg cabbage, beans), diary
• Coffee – stimulant to colon
• Fructose – natural sources + as additives
• Oligosacchardides – in fruits and sweetening agents (sorbitol)
• Rice-based diet least likely to cause wind
5. Anti-depressants
• Low dose TCA – eg amitryptyline 10-20 mg nocte (effect via pain modulation effect and by slowing bowel transit)
• SSRIs – may be more helpful if constip predominant


Nausea Feeling of imminent vomiting
Vomiting Forceful expulsion gastric contents – integrated reflex involving autonomic and somatic nervous sys
Retching Different motor act from vomiting; gastric contents oscillate betw stomach and esophagus
Regurg Food is bought back into mouth w/o motor or autonomic activity
Free regurg – suggests severe GOR
Regurg of undigested foods suggests partial esophageal obstr
Anorexia Loss of desire to eat; non-specific sx – could be related to malignancy, depr, GI dis or metabolic d/os
Fear of eating due to expected abdo discomfort is a specific sx which suggests sub-acute bowel obstr
Early satiety is a feeling of being full after eating a small quantity of food; usu part of functional dyspepsia but can be due to gastric ca
Chronic belching – due to excessive swallowing of air, may be caused by excessive salivation (due to smoking, oral irritation or chr GOR), by anxiety or habitual

Acute onset N/V
Consider other sxs -
• Diarrhea – gastroenteritis or food poisoning
• Acute abdo pain – nature of pain impt, some conditions are particularly assoc w n/v eg biliary colic
• Faeculent vomiting and abdo distension suggest bowel obstr
• Vertigo – labyrinthine probs

Chr N +/- V
1. Meds
• Digoxin, Theophyliline – common cause in elderly
• Erythromycin – RUQ pain + vomiting
• Nitro-imidazoles – w alcohol
• Methotrexate, azathioprine, chemo drugs
2. Non-GI Causes
• Pregnancy
• Any severe localised pain
• Migraine (distinguished from tension headache by n/v)
• Projectile vomiting or spontaneous vomiting w/o nausea suggest ↑ ICP
• Chr vomiting immed after meal where no suggestion of organic dis → eating d/o
• Non-organic vomiting w/o eating d/o → response to stress (clue = repeated vomiting in absence of weight loss)
• Chr nausea as a sole sx usu functional in nature → depr
3. GI Causes
• Severe regurg (GORD) can be mistaken as vomiting
• Vomiting occurring immed on awakening → alcoholism
• Vomiting non-digested food soon after meal suggests esophageal dis such as a diverticulum, achalasia or stricture
• Vomiting occurring 3-4 hrs after meal esp assoc w partially digested food → gastric outlet obstr
• Sx complex of nausea, fullness, upper abdo distension + early satiety → part of spectrum of functional dyspepsia
• LT DMT1 → diabetic gastroparesis
• Anorexia + early satiety + nausea → ? gastric ulcer or ca

Consequences of vomiting
• Sudden forceful vomiting → traumatic tearing esophageal mucosa → haematemesis (Mallory-weiss lesion) – most common cause in younger pt
• Younger pt after excessive alcohol intake or gastroenteritis
• Complete perforation of esophagus → sudden severe CP, recog often delayed, high mortality, v rare
• Repeated vomiting → dehydration, hypokalemic/hypochloraemic metabolic alkalosis (rarely seen today, except in childr w pyloric stenosis)
• Aspiration – if diminished conciousness, excessive alcohol intake or drug overdose

a. IVF – correct dehydration
b. Sx tx often undertaken when underlying condition unknown or cannot be treated superficially
i. Phenothiazines – chlorpromazine, prochlorperazine (stemetil), haloperidol
• Act directly on chemoreceptor trigger zone in brainstem
• S.eff – sedation, hypotension, extrapyramidal d/os
• Widespread use in tx of n/v; esp effective in palliative setting where nausea may be related to underlying malignancy + narcotic/radiation effects
ii. Metoclopramide (Maxalon) and Domperidone (Motilium)
• Stimulate gut motility → acceleration of gastric emptying
• S.eff – extrapyramidal reactions (avoid in children/elderly)
• Useful in tx of migraine as delayed gastric emptying is part of spectrum of illness
iii. Anti-cholinergics – Atropine, Hyoscine (Buscopam), Cyclizine (Marzine)
• Less anti-emetic properties; used primarily in prevention of motion sickness
• S.eff – dry mouth, blurred vision
• Scopolamine (transdermal prep) appears to be more acceptable
c. Motility-type dyspepsia (assoc w upper abdo bloating + postprandial fullness) → domperidone
d. Cytotoxic induced nausea (esp w agents such as cisplatin) → ondansetron (5HT3 antagonist) is better but more expensiv


• Peak incidence DU 1940-60 then gradual ↓ - due to ↓ rates of inf w H.pylori.
• In general, DU>GU (but more NSAID related GU in elderly.
• Rates of ulcer complications risen in elderly (esp F) – both hemorrhage and perforation (?due to ↑ NSAID use in elderly)

Predisposing Factors
• Helicobacter pylori infection
• Gastric acid secretion – 2x ↑ in DU, normal to low acid secr in GU
• Smoking - ↑ rate ulcer recurrence, delayed ulcer healing
• NSAIDs – 3-4x ↑ risk, strong assoc w hosp adm w hem, 15x ↑ risk w NSAIDs + Steroids combined
• Impaired mucosal damage - ↓ duodenal bicarb secr, abnormal mucus, ↑ back diffusion H+, low mucosal PGs – mainly an issue w NSAID tx
• Zollinger-ellison syndr (Gastrinoma) – v rare, suspect if aggr ulceration, elev serum fasting gastrin (off PPI)

• Epidem
• Inf acquired in childhood → lifelong inf → chr gastritis in all affected individuals → 5-10% will then develop ulcer dis
• Inf risk – related to c/hood living conditions (esp no. children in house, SES)
• NZ – 20-30% of adults (age dependent) infected, 5% of children (cohort phenomenon, changing living standards), proportion of infected individuals falling
• ↑ M/PI
• Associations of H.pylori infection
• Antral gastritis >95% H.pylori pos
• DU 90%
• GU 70-80% (other 20-30% are NSAID related ulcers)
• Gastric ca 3x ↑ risk
• MALTma Rare, malignant expansion of mucosa-assoc lymphoid tis, 80% assoc w H.pylori, most will regress w H.pylori eradication tx
• Dx tests (based on detecting bacterial urease enzyme activity)
• Urea → ammonia + CO2 (ammonia gives alkali pH (detected by indicator dye), labelled CO2 detected in expired air)
 CLO test (rapid urease test)
• ?Serology → ?gG
• ?13C (stable isotope) – most accurate test
• Endoscopic biopsy + istology
• Faecal antigen test – useful post Rx
• Pathogenesis of H.pylori related diseases
• Devt of DU assoc w gastric metaplasia in duodenum (assoc w high acid output states)
 High acid output could be due to sustained hypergastrinaemia (due to H.pylori induced stim of antral G cells) or genetic (↑parietal cell mass)
 H.pylori migrates from antrum to duodenal cap causing mucosa breakdown
• GU diff pway
 Pangastritis → chr atrophic gastritis (conseq of LT inf w H.pylori) → unstable mucosa
 Atrophic gastritis + intestinal metaplasia are RFs for gastric ca
• Tx
• Eradiation of H.pylori – Triple therapy (Omeprazole 20 mg bd + clarithromycin 500 mg bd + either amoxicillin 1g bd or metronidazole 400 mg bd if allergy)
• 90% eradication rate
• <2% recurrence rate
• For GU → repeat endoscopy to confirm healing + biopsies to excl malignancy

NSAID Ulcers
• Tx
• Stop NSAID
• LT prophylaxis if continuing NSAID – PPI or Misoprostol both ↓ incidence of gastroduodenal ulceration (PPI better tolerated + od dosing)
 Misoprosolol → diarrhea (30%), multiple daily dosing, rarely used
• Prevention of NSAID ulcer complications
 COX2 antagonists – lower risk GI ulceration, PPI prophylaxis not reqd, incr risk MI

Complications of PU Disease
1. GI Bleeding
2. Perforation
3. Pyloric obstruction

• Dx
• B/ground sxs of PU dis except if NSAID related
• Sudden onset, severe constant upper abdo pain which generalises to whole abdomen
 Note where pain starts - Epigastric (cf. perforating sigmoid diverticular dis - LLQ)
• Exmn findings depend on delay to pres
• Early – some tenderness, tachycardia
• Late – rigid peritonitis, shock
• Ix – erect CXR, free air under diaphragm (crescent sign)

Pyloric Obstruction
• Less commonly due to PU dis, dx now usually gastric ca
• Dx
• Vomiting – often several hours after meals, may be recognisable food from previous days
• Exmn – dehydration, epigastric fullness, succussion splash
• Ix – gastroscopy with biopsy (check for malignancy)
• Tx
• Large NG tube → empty stomach
• Fluid resus → correct metabolic alkalosis
• PPI – some of the obstr may be due to active ulceration causing spasm + edema superimposed on scarring from chr dis
• Surgical Tx - If no improvement after 5-7 days (rare w H.pylori related obstr), surgery indicated → partical gastrectomy w bilroth 11 reconstruction
 Duodenal stent (self expanding metal stent) if dx of ca

Gastric Surgical operations
• Truncal vagotomy w drainage procedure – either pyloroplasty (widening of pylori canal and any adjacent duodenal stricture by longitudinal incision) or gastrojejunostomy (establishment of direct communication betw stomach and jejunum)
• Highly selective vagotomy – parietal cell
• Antrectomy and vagotomy – proximal gastric remnant re-anastomosed to duodenum (billroth 1) or by bringing up a loop of prox jejunum as a gastrojejunostomy (billroth 11)

Complications of Gastric Surgery
1. Post-vagotomy diarrhea
 Some degree of diarrhea 20% of pts after truncal vagotomy (TV)
 Anti-diarrhea tx in 10%
 Serious problem in 1%
2. Dumping syndrome
 1-2% of pts after gastrectomy
 sxs are CV and GI – palpitations, sweating, dyspnea, flushing, cramps, syncope
 Early dumping – due to rapid load of hyperosmolar chime into jejunum → hypovolaemia
 Late dumping – due to hypoglycaemia when high carb load results in excessive insulin release
3. Bilious vomiting
 May be treated with prokinetics
 Rarely will need revision with Roux-en-Y reconstruction
4. Late metabolic sequelae
 Weight loss
 Anemia – usu Fe deficiency from decr intake, poor absorption or ?blood loss
 Bone dis – both osteomalacia (decr vit D) + osteoporosis


Standard film = Supine AP
Other films = erect (fluid levels), lateral decubitus (free air), erect chest (free air)


2 c/ments – Intra-peritoneal and Retro-peritoneal (aorta, kidneys, psoas mus, part of duodenum).
Ex. A ruptured AAA bleeds into retroperitoneal c/ment causing loss of the iliopsoas shadow.
L kidney should be higher than R kidney.
L4/5 junction → top of iliac crest.
L4 → aorta bifurcation.
T4 → arch aorta.

Densities Organs → Grey
Bowel → lucent (air), feces, grey (mucosal border)
Bone → white

1. GAS Normal gas distribution - Stomach (always), SB (2-3 loops non-distended), LB (almost always in rectum/sigmoid)
Normal fluid levels – Stomach (always except supine), SB (2-3 loops sometimes), LB (usu none)

1. SBO

Small Bowel Identification
• Central
• Small calibre (<3cm)
• Thin mucosal folds; valvulae extend across lumen
Normal Radiology
• Minimal gas present (2-3 loops non-distended).
Key Radiological Features
• multiple dilated loops of SB (distension = >3cm)
• large bowel non-distended
• no air sigmoid/rectum
• disproportionate SB dilation
• Air fluid levels on erect
• Sausages, string of beads of sign
• N/V
• Ø flatus/wind
• Abdo distension (percussion resonance)
• Tenderness
• Tinkling b/s
1. Adhesions
2. Hernias
3. Volvulus
4. Cancer
5. Gallstone ileus
6. Strictures – crohns, ischemia
7. Intussecption
1. If previous surgery → dx adhesions → proceed to surgery
2. If Ø previous surgery or atypical presentation → proceed to CT

2. LBO

Large Bowel Identification
• Peripheral
• Thick haustral folds not extending across lumen
• Large diameter 5-6cm
• Faeces present
Key Radiological Features
• Dilated colon to point of obstruction
• Air in LB → dilation (>6cm Transverse Colon, >9cm Caecum)
• Ø air in sigmoid/rectum
• Ø air in SB (except if ileocecal valve incompetence; beware – may cause LB decompression into SB resembling SBO)
1. Bowel cancer
2. Caecal or Sigmoid volvulus (both caecum and sigmoid on a mesentery and vulnerable to volvulus) – esp if v dilated colon
3. Hernia
4. Diverticulitis
5. Intussception
• Risk of caecal perforation
• Colonoscopy
• CT
• Barium studies


Key feats
• air in sigmoid/rectum (distension)
• multiple distended SB loops
• air in LB
• Absent or hypoactive b/s

Paralytic/Generalised Ileus
Key Features
• Gas in dilated SB or LB/Rectum
• Long air fluid levels
• Diffuse gas extension S1-L1
• Post-op
• Trauma
• Meds
• Peritonitis
• Electrolyte imbalance

Localised Ileus
Key Features
• 1-2 persistently dilated loops of SB or LB
• Gas in rectum/sigmoid
Pitfalls – may resemble early SBO
Sentinel loop sign → location impt, appendicitis, pancreatitis, cholecystitis, diverticulitis

SIGNS OF FREE AIR (Intra-abdominal / Intra-peritoneal air)

Crescent sign – air beneath diaphragm
Riglers sign – both sides of bowel wall visible
Falciform ligament sign
Causes Rupture of hollow viscus – perforated ulcer/diverticulitis/carcinoma or trauma/instrumentation or post-op 5-7 days
NOT ruptured appendix


Description of Stones
• Single / Multiple
• Homogenous / Heterogenous
• Opaque / Lucent / Laminar
• Spherical / Round / Regular / Irregular

a. Rim-like – wall of hollow viscus (cysts eg renal cyst, aneurysm eg AAA, secular organ eg GB).
b. Linear/track-like – walls of a tube (ureter, arterial wall).
c. Lamellar – formed in lumen of hollow viscus (renal stones, gallstones, bladder stones).
d. Cloudlike/amorphorous – formed in solid organ or tumor (leiomyomas, ovarian cyst adenoma).

Chr pancreatitis – small dots scattered throughout pancreas.
Phleboltihs – pelvic v calcifications, normal, benign, well defined, round, in pelvis (cf renal/ureteral calculi less well defined, no lucency in centre, higher)
AAA – linear calcification (atherosclerosis).
Appendicalth – laminar (pearl/bullseye) RLQ → will have appendicitis in lifetime, RLQ pain + Appendicalth = Appendicitis.
Bony mets – lucent or sclerotic or both



1. Oropharyngeal dysphagia (difficulty initiating swallowing)
a. Etiology
i. Neuro – CVA, Parkinsons, MND
ii. Local – extrinsic compression, neoplastic
iii. Motility – hypertensive UES, incomplete UES relaxation, premature closure of UES (likely cause of a zenker diverticulum aka pharyngoesophageal)
b. Mgt
i. Videofluroscopy
ii. SLT – altered food consistency, bolus size, safe swallow techniques
iii. Cricopharyngeal myotomy
iv. Closure of zenkers diverticulum
2. Esophageal dysphagia (food sticking)
a. Intermittent sxs - solids only
i. Etiology
1. Schatzki’s ring (fibrous ring at gastro-esophageal junction) → steakhouse syndr
2. Mild peptic stricture
3. +/- motility d/o
ii. Ixs – radiology or endoscopy
iii. Mgt - dilation
b. Intermittent sxs - solids and liquids
i. Etiology → motility disorder
1. Non-specific motility d/o (impaired esophageal peristalsis) → Ltd tx options
2. Esophageal spasm w cp → ensure not cardiac cause of cp, nitrates or CCBs (sublingual or oral)
3. Achalasia – absence of LOS relaxation + ↓ / absent peristalsis
a. Radiology – impaired peristalsis, dilated esophagus (food/saliva), intermittent passage narrow jet of barium
b. Manometry – most accurate and sens test
c. Tx
i. Endoscopic dilation to disrupt LOS
ii. Laparoscopic cardiomyotomy
iii. Botulinum toxin injection into LOS → ~1 year effect
c. Progressive sxs
i. Ixs – urgent, endoscopy preferred as direct vision and biopsies can be taken
ii. Peptic esophageal stricture – tx w dilations + maintenance PPIs
iii. Esophageal carcinoma – older, weight loss, more progression to dysphagia, heavy alcohol/tobacco use
d. Odynophagia (pain on swallowing) – commonly caused by peptic esophagitis or infective esophagitis

Heartburn (GE Reflux)

1. Definitions
a. Heartburn – retrosternal burning discomfort
b. GE Reflux – abnormal exposure of esophagus to gastric contents (+/- sxs)
c. Reflux esophagitis – ulceration and inflammation of lower esophagus 2ndry to reflux
d. GE reflux dis – includes all clinically relevant manifestations of reflux
2. Epidemiology – 35% 1/month, 7% daily
3. Pathophysiology
a. Transient relaxation LOS – normal post prandial reflex to allow gas to escape from stomach, Ø occur in supine position
i. Majority of reflux episodes occur during this transient relaxn
b. Low mean LOS pres – reflux episodes occur with ↑ abdo pres, bending, supine, gastric distension
c. Hiatus hernia – LOS above diaphragm, thus less effective barrier and assoc w reflux
4. Sxs
a. Typical – hearburn, regurg, belching, waterbrash
b. Warning – dysphagia, odynophagia, anemia, weight loss
5. Ixs
a. Endoscopy – Normal in ~50% w reflux, Presence of reflux esophagitis diagnostic
b. Ambulatory 24 hr esophageal pH study – helpful if sxs troubling but endoscopy normal, correlate pain to acid exposure helpful
6. Patterns of Reflux disease
a. Mild disease (majority)
i. Normal LOS pres, intact sphincter mechanism, mostly post-prandial upright reflux assoc w transient LOS relaxn
ii. Freq short lived reflux episodes
b. Severe or complicated disease
i. Hiatus hernia or low LOS pres
ii. Free passage of refluxate when supine or when sleeping
c. Hypersensitive esophagus
i. Normal esophageal acid exposure (normal pH study)
ii. But incr sensitivity to acid, assoc w IBS
d. Functional heartburn
i. Sxs suggest reflux but normal pH study and Ø correlation of sxs w reflux episodes
ii. Commonly fail PPI tx, Unknown pathophysiology
7. Mgt
a. Lifestyle – Ø smoking, weight reduction
b. Antacids – largely ineffective
c. H2 Antagonists – effective for mild dis, best choice when PRN meds reqd as rapid onset
d. PPI
i. More effective control of secretion over 24 hrs, single morning dose usu sufficient
ii. Failure to respond
1. Inadequate acid suppression - ↑ dose to bd, 30 mins prior to meals, add H2 antag at bedtime
2. Hypersensitive esophagus – ↑ dose, addition of low dose TCA, explanation and reassurance
3. Wrong dx – angina, achalasia, esophageal spasm, IBS, gallstones
e. Surgical – laparoscopic fundoplication +/- cruroplasty
i. Indications – avoidance of LT PPI meds, med tx ineffective
ii. Complications – may aggravate bloating/flatulence (inability to belch), dysphagia common for initial 3-6 months
8. Complications of Reflux
a. Barretts esophagus – Squamous to columnar epithelium (pre-malignant condition related to acid expos)
i. ↑ risk esoph adenocarcinoma


1. Dyspepsia – upper abdo discomfort >2 weeks
2. Etiology
a. Functional dyspepsia (most common) – unknown pathophysiology, normal gastroscopy/US, no response to PPI tx
i. Sxs may be related to delayed gastric emptying
b. GERD – some pts get dyspepsia, not heartburn
c. PU dis
3. Ixs
a. Emperic trail – PPI (often successful)
b. Gastroscopy – dx of reflux esophagitis, biopsy suspiciou lesions, H.pylori testing
c. Barium meal – only if dysphagia
d. Upper abdo US – to exclude biliary colic (gallstones), for more discrete and severe episodes of upper abdo pain
4. Mgt of functional dyspepsia
a. Reassurance re absence of pathology
b. Domperidone (motilium) may help post-prandial bloating, fullness, nausea
i. Dopamine antagonist with anti-emetic properties → gastrokinetic effects + antagonism of Da Rs in chemo-recep TZ
ii. Effects → ↑ esoph pres, improved antroduodenal motility, accelerates gastric emptying
c. Tx of H.pylori in absence of ulcer dis

Peptic Ulcer Disease

1. Epidemiology
a. ↓ rates of H.pylori ulcers
b. ↑ rates of complications in the elderly (? NSAID related)
2. Predisposing Factors
a. H.pylori infection
b. NSAIDs – 3-4x ↑ risk (15x ↑ risk if NSAIDs + steroids)
c. Gastric acid secretion – 2x ↑ risk for DU
d. Smoking - ↑ rate of ulcer recurrence, delayed ulcer healing
3. H.pylori
a. Epidemiology – acqd in childhood, related to living conditions, NZ 20-30% of adults, 5% of children
b. Associations
i. Gastritis >90%
ii. DU 90%
iii. GU 70-80% (remainder NSAID related)
iv. Gastric carcinoma – 3x ↑ risk
c. Ixs
i. Non-invasive
1. Urea breath testing
a. Based on hydrolysis of urea into ammonium and CO2 by H.pylori
b. Example – non-radioactive 13C test
c. False negatives common in pts on antibiotic and PPI therapies
2. Serology
a. IgG antibodies
b. Reduced accuracy
3. 13C bicarbonate assay
a. Measuring two serum sample, one taken prior to and the other after a 13C urea rich meal
4. Fecal antigen test
ii. Invasive → Endoscopic biopsy
1. CLO - Rapid urease test
2. Histology
d. Tx → Triple therapy – omeprazole 20 mg bd + clarithromycin 500 mg bd + amoxicillin 1g bd
i. 90% eradication
ii. GU requires repeat endoscopy to confirm healing and exclude malingancies
4. Mgt of NSAID Ulcers
a. Stop NSAID
b. Or - LT prophylaxis with PPI
c. Or – switch to COX2 antagonists
5. Complications of PU disease
a. GI bleeding (hemorrhage)
b. Perforation and peritonitis
i. Presentation
1. Sxs – sudden onset, severe, constant upper abdo pain generalising to whole abdomen
2. Early signs – tenderness, tachycardia
3. Late signs – rigid peritonitis, shock
ii. Ixs – free air under diaphragm on erect cxr (crescent sign)
c. Pyloric obstruction
i. More likely due to gastric ca than PU dis
ii. Pres
1. Vomiting (recognisable food from previous days)
2. O/E – dehydration, epigastric fullness, succession splash
iii. Ixs – gastroscopy with biopsy (to exclude malignancy)
iv. Tx
1. NG tube → empty stomach
2. IVF + correction of metabolic alkalosis (due to vomiting)
3. PPI → ?some of obstr due to active ulceration causing spasm + edema superimposed on chr scarring
4. Surgical → read if no improvement after 5-7 days (rare when H.pylori related)
a. Partial gastrectomy with billroth 11 construction
b. Duodenal stent – if ca
6. Complications of gastric surgery
a. Post-vagotomy diarrhea
b. Dumping syndrome
i. Early → hypovolaemia due to hyperosmolar chime into jejunum
ii. Late → hypoglycaemia from excessive insulin response to high carb load

Nausea and Vomiting

1. Definitions
a. Nausea = feeling of imminent vomiting
b. Vomiting = forceful projection of gastric contents
c. Retching = contents oscillate between gastric and esophageal contents (different mechanism to vomiting)
d. Regurgitation = food back into mouth
e. Anorexia = loss of desire to eat
2. Acute N/V – consider other sxs:
a. Diarrhea → gastroenteritis
b. Acute abdo pain → biliary colic
c. Faeculent vomiting + abdo distension → bowel obstruction
d. Vertigo → labyrinthine problems
3. Chronic N/V
a. Medications – eg erythromycin, methotrexate, chemo drugs
b. Non-GI causes
i. Pregnancy
ii. Any severe localised pain
iii. Migraine
iv. ↑ ICP → projective or spontaneous (Ø nausea) vomiting
c. GI causes
i. Severe regurg, not vomiting
ii. Vomiting non-digested food soon after meal → diverticulum, achalasia, stricture
iii. Vomiting 3-4 hrs after meal, partial digested food → gastric outlet obstruction
iv. Functional dyspepsia spectrum → nausea, fullness, upper abdo distension, early satiety
4. Consequences of vomiting
a. Hematemesis – Mallory-weiss tear if young and alcohol consumption or gastroenteritis (traumatic tear esophageal mucosa)
b. Repeated vomiting – dehydration + hypokalemia + hypochloraemia + metabolic alkalosis
c. Aspiration – if ↓ LOC
5. Management
a. IVF – correct dehydration
b. Anti-emtics
i. Phenothiazines – chlorpromazine, prochlorperazine (stemetil), haloperidol
1. act directly on chemoreceptor trigger zone in brainstem
ii. Metoclopramide (maxalon) and Domperidone (motilium)
1. Stimulate gastric motility, accelerate gastric emptying
iii. Anti-cholinergics – atropine, hyoscine (buscopam), cyclizine (marzine)
1. Less anti-emetic properties, used for motion sickness
c. Functional dyspepsia → domperidone
d. Cytotoxic induced nausea → ondansetron


1. Epidem – 15-20% across all ages, F>M
2. Presentation
a. >3 months of abdo pain, relief w defecation
b. assoc ∆s in stool consistency or frequency, alternating diarrhea/constipation is common
c. urgency
d. bloating
3. Red flags
a. Nocturnal diarrhea or abdo pain
b. Rectal bleeding
c. Weight loss
d. High vol stool (>200 mls) >4 weeks
e. Stool consistency suggesting malabsorption – pale, greasy, offensive, tends to float, difficult to flush
4. Pathophysiology
a. Abnormal muscle/motor activity of SI and colon
b. Visceral hypersensitivity
5. Ixs
a. Bloods – FBC, iron studies, ESR, LFTs, Celiac antibodies, folate/b12 deficiency
b. Sigmoidoscopy
c. If >40 yrs age or recent unexplained ∆ in bowel habit → colonoscopy or barium enema
6. Mgt
a. Explanation + Reassurance – explained as overactive or oversensitive gut, Ø dis
b. Ixs may help alleviate anxieties or fear
c. Dietary
i. Exclulde gas forming foods – wheat, cabbage, beans, diary
ii. Exclude coffee – colon stimulant
iii. Fructose
iv. Rice based diet less likely to produce wind
d. Therapeutics
i. Fibre supplements – may help constipation + incomplete evac, may aggravate bloating
ii. Laxatives for constipation sxs – kiwifruit
iii. Loperamide for diarrhea sxs
iv. Anti-spasmodics – benefit for abdo cramps (eg mebeverine is an anti-cholinergic)
e. Anti-depressants – amitriptyline 10-20 mg nocte

Chronic Diarrhea

1. Definition of diarrhea
a. ∆ in consistency – semi-formed, watery
b. Freq >3/day
c. Vol/weight >200g/day
2. Types of diarrhea
a. Secretory - ↑ active secretion or inhibition of absorption, Ø structural damage
i. Ex. Cholera – toxin stimulates Cl secretion → Na and water follow
b. Osmotic – water loss due to heavy osmotic load, as occurs in maldigestion where nutrients in lumen pull water across
i. Ex. Celiac disease
c. Motility-related – food moves too quickly, meaning insufficient time for nutrient and water absorption
i. Ex. Post vagotomy
d. Inflammatory – damage to mucosal lining leading to passive loss of protein-rich fluids and ↓ ability to absorpb lost fluids
i. Ex. Bacterial or viral infections, IBD
3. Effects of stress on the gut → churning sensation
a. ↓ gastric motility (vagus inhibition)
b. ↑ colonic motility (↑ sacral parasym excitation)
4. Conditions causing malabsorption
a. Celiac disease
b. Microscopic colitis → watery diarrhea, normal colonoscopy, microscopic colitis of unknown cause
c. Tropical sprue → post infective, subtotal villous atrophy – persisting diarrhea + macrocytic anemia
d. Bacterial overgrowth in SB → ↑ conc of bacteria in jejunum due to ↓ gastric acid secr / ↓ SB motility etc
i. Pres – diarrhea, weight loss, megaloblastic anemia
e. SB resection
5. Celiac Disease
a. Epidem – most common cause malabsorption, predominantly european 1/100
b. Pathogenesis
i. Gluten → abnormal cellular + humoral response to gliadin (component of gluten) → mucosal damage
ii. Exposure of immunologically active epitope requires tis transglutaminase (an extracellular matrix enzyme)
c. Pathology → villous atrophy + crypt hypertrophy + intraepithelial lymphocytes
d. Pathophysiology
i. Loss of brush border enzymes → loss of stimulus for pancreatic + bile secretion
ii. Exudation of protein across denuded mucosa
e. Presentation
i. Childhood → FTT, diarrhea, irritable, Fe deficiency, abdo distension etc
ii. Adult
1. Relatively asx - mild bloating, abdo discomfort, ↑ wind
2. Diarrhea
3. Borborygmi (rumbling, gurgling noises produced by mvment of gas/fluid in gut audible at a distance)
4. Weight loss common
5. Anemia – iron or folate deficiency
6. Nutritional deficiencies – eg bruising (vit k), tingling (calcium)
f. Ixs
i. Endomysial antibody (IgA) and tissue transglutaminase (tTG) → 95% accurate
ii. Gastroscopy + distal biopsy → confirmation of dx
g. Tx
i. Gluten free diet – avoid products made from wheat, rye and barley
ii. Specific dietary supplements may initially be reqd – Fe, Folate, Vit D
h. Complications
i. Intestinal lymphoma
ii. Osteoporosis – if dx >40 yrs age → check bone density


1. Etiology
a. Dietary
b. Colonic slow transit times – main cause of severe idiopathic constipation in adults
c. IBS
d. Drugs – opiates, CCBs, anticholinergics
e. Depression, anxiety
f. Hypothyroid
g. Hirschsprung’s dis (segmental absence of myenteric nerves – usu presents in infancy, occasionally in adults)
2. Management Ladder
a. Diet → water
b. Kiwifruit
c. Metamucil or Normacol (fibre supplements)
d. Lactulose – 10-20 mls bd prn
i. Synthetic sugar as a yellow-orange syrup used in tx of constipation
ii. Its metabolites draw water into bowel, can take up to 24-48 hrs to work
iii. Side effects – abdo cramping, gas, borborygmus, flatulence
e. Coloxyl and Senna – 1 or 2 bd
i. Coloxyl = stool softner, generally unhelpful, useful for painful anal conditions
ii. Senna = stimulant laxative
f. Movicol sachets bd prn (colonoscopy lavage sachets – osmotic laxative) – generally ST agents (alternatively Mg2+ salts)
3. Ixs – reqd if no improvement
a. Serum calcium, TFTs
b. Plain axr – assess degree of fecal loading, check for dilated colon (megacolon)

Approach to abdominal pain

1. Acute abdo pain
a. Acute pancreatitis
b. Acute diverticulitis
c. Acute cholecystitis
d. Peritonitis
e. SBO
f. LBO
g. Ectopic pregnancy
2. Chronic intermittent pain
a. Dyspepsia/Reflux – upper abdo/retrosternal, related to meals
b. DU – epigastric, worse on empty stomach
c. IBS – usu lower abdo, variable bowel habit
d. Diverticular dis – LLQ pain, relieved by flatus, bm
e. Constipation – lower abdo cramping, generalised distension, bloating
f. MS – thoracic sp, n entrapment
g. Inflammation dis of colon – esp CD w peritoneal irriation or subacute obstr
h. Pelvic pain – endometriosus, ovarian path, tubal sepsis (PID)
3. Chronic infrequent pain
a. Biliary colic – discrete episodes RUQ pain lasting 2-8 hrs
b. Renal colic – loin to groin
4. Chronic unrelenting pain
a. Abdo malignancy – esp pancreatic ca or liver mets
b. Thoracic pain – referred from # or mets
c. Chr pancreatitis


1. Epidemiology
a. ↑ incidence of CD
b. CD common among nth Europeans, rare in developing countries
c. Smoking - ↑ risk CD, ↓ risk UC
2. Etiology
a. Unknown
b. Genetic – 8% lifetime risk if first degree relatives (30x ↑ risk)

Ulcerative Colitis
3. Definition – chr inflammatory dis of unknown cause characterised by ulceration of the colon and rectum
4. Pathology
a. Diffuse mucosal inflammation only
b. Neutrophil infiltrate through crypt epithelium → crypt abscess (chr inflame cells, loss of goblet cells, paneth cell metaplasia)
c. LB only
d. Spreads proximally from rectum
e. Continuity
5. Hx – relapses and remession of:
a. Diarrhea +/- blood
b. Freq boel motions +/- tenesmus/urgency
c. LLQ discomfort
d. Fever
e. Malaise
f. Weight loss
6. Ixs
a. Bloods - ↑ ESR
b. AXR – colon dilation
c. Colonoscopy + biopsy – extent + severity of dis
7. Differentials
a. Infective colitis – Camplyobacter jejuni, salmonella
b. Colonic CD
c. Pseudomembranous colitis – C.difficile
d. Ischemic colitis – elderly pts w vascular dis
8. Mgt
a. Acute attack
i. Rectal steroids +/or 5-ASA (5-aminosalicytic acid / masalazine) foam/liquid enema/suppository
ii. Oral 5-ASA (mesalazine) - Pentasa, Asacol
b. Moderate to severe attack
i. Add oral steroids
ii. If no response → IV hydrocortisone
c. Severe attack (>6 b/m per day, fever >37.5, ESR >30, albumin <30)
i. Add oral/iv cyclosporine
ii. Watch for complications – toxic megacolon, perforation and bleeding
d. If ineffective
i. ?Infliximab (monoclonal antibody to TNF)
ii. Colectomy with ileostomy or ileo-anal anastomosis and ileal J pouch
9. Prognosis
a. 90% remit after first episode, but recurrent episodes common
b. Maintenance
i. Sulphasalazine
ii. Mesalasine
iii. Azathioprine (if requirement for frequent or prolonged courses of prednisone)

Crohn’s Disease
1. Definition
a. a chronic enteritis of unknown cause typ involving the terminal ileum + other parts of the GI tract
b. characterised by patchy deep ulcers that may cause fistulas + narrowing/thickening of bowel by fibrosis + lymphocytic infiltration
2. Pathology
a. Any part of GI tract
b. Begins as aphthous ulcers within epithelium overlying lymphoid aggregates
c. Ulceration → fissuring + deeply penetrating
d. Mucosal inflammation betw fissuring → cobblestone appearance
e. Discontinuous (skip lesions)
f. Peri-anal manifestations
g. Transumural inflammation, submucosal fibrosis, non-caseating granulomas
3. Hx – variable, depending on what part of GI tract affected:
a. Terminal ileum → RIF pain
b. Colonic → bloody diarrhea, cramping lower abdo pain
c. Rectal → urgency, incontinence, bleeding
d. Perianal dis → pain + d/c due to abscess/fistulae
4. Differentials
a. Colonic → UC
b. Ileo-colonic → TB, appendix abscess, caecum carcinoma, lymphoma
c. Sigmoid → diverticular dis
5. Ixs
a. Colonoscopy/Ileoscopy
b. SB enema
c. CT – if suspected abscess/fistula
6. Tx
a. Dietary supplements
b. Medical tx
i. Steroids – 40 mg od ↓ over 6-8 wks with clinical improvement
ii. 5-ASA → eg Pentasa
iii. Immunosuppressives → aziothriprine, methotrexate (steroid sparing agents)
iv. Infliximab → effective in acute severe dis, maintenance tx effective but limited by cost
c. Surgical draining of intra-abdominal pus
i. B/spec A/B cover – metro + ciprofloxacin
d. Surgical resection / stricturoplasty
i. Indications – failed med tx, unacceptable side effects from tx, complications
ii. Resection not curative – recurrence post surgery common
1. Minimised with azathioprine + high dose 5-asa (pentasa) + metro following surgery
iii. Minimise resections
7. Complications in IBD
a. Intestinal obstruction – subacute
b. Fistulae – bowel to bowel, bladder, vagina or ant abdo wall
c. Systemic feats – similar to UC
d. Nutrional deficiencies
i. Anemia – iron or folate deficiency, chr dis, blood loss
ii. Hypoproteinemia – protein loss, malnutrition
iii. Malabsorption – fat sol vitamins (adek), vit b and c
iv. Osteoporosis – steroids, low dietary calcium

Comparisons of various factors in Crohn's disease and ulcerative colitis
Crohn's disease Ulcerative colitis
Terminal ileum involvement
Commonly Seldom
Colon involvement Usually Always
Rectum involvement Seldom Usually
Involvement around the anus
Common Seldom
Distribution of Disease Patchy areas of inflammation Continuous area of inflammation
Endoscopy Deep geographic and serpiginous (snake-like) ulcers
Continuous ulcer
Depth of inflammation May be transmural, deep into tissues Shallow, mucosal
Common Seldom
Common Seldom
Autoimmune disease
Widely regarded as an autoimmune disease No consensus
Surgical cure Often returns following removal of affected part Usually cured by removal of colon
Higher risk for smokers Lower risk for smokers

GI Bleeding

1. Immediately on presentation
a. FBC (anemia)
b. U/E
c. INR (bleeding tendency)
d. Renal function
e. LFTs – hypoalbuminemia, vit k deficiency (CF deficiency), cirrhosis
f. Blood for x-match
2. Hx
a. Haematemesis –
b. Malaena – black tarry motions
c. Anemia – implies subactue blood loss (tiredness, weakness, SOB on exertion) - <8 hrs
d. Causes – NSAIDs or aspirin, reflux or ulcer like sxs, liver dis + potential for esophageal varicies
i. Point prev of GU/DU in NSAID users ~20%, ↑ risk 4-5x
ii. Risk factors for nsaid complications – age >75, past hx ulcer/dyspepsia, anticoagulants, steroids
3. Upper GI bleeding
a. Etiology
i. DU or GU
ii. Gastric erosions
iii. Esophagitis
iv. Esophageal varicies
v. Mallory-weiss tear
b. Risk prediction
i. Age >80
ii. Sys BP <100
iii. Major co-morbidities – eg HF, IHD, RF, LF, Mets
c. Mgt principles for high risk pts
i. X-match 4-6 units whole blood
ii. Resus fluids
iii. NBM
iv. IV Omeprazole Q12H (due to risk of ulcers)
v. Endoscopy ixs
d. Tx of bleeding ulcer
i. Endoscopy + injection sclerotherapy (if large ulcer, visible vessel or active bleeding)
ii. Surgery for uncontrolled bleeding after 2 endoscopic attempts
e. Prognosis
i. Overall mortality 5-10% (death usu from other cause eg liver dis, multisystem illness, malignancy)
ii. Bleeding varices – 40% mortality
4. Lower GI bleeding
a. Etiology
i. Divertiular disease – 50%
ii. Neoplasm – 10%
iii. Colitis – 10%
b. Mgt
i. Iron deficiency anemia + no obvious source of blood loss → MUST evaluate upper and lower GI tract
ii. Colonoscopy ixs
iii. Surgery rarely reqd unless resection of colonic malignancy reqd
5. Anemia
a. Losses >5-10 mls/day will cause an iron deficiency anemia
b. >200 mls blood reqd to cause malaena
c. Etiology
i. reflux esophagitis, gastroduodenal ulceration
ii. tumors – carcinoma of colon or large colonic polyps
iii. Other – CD/colitis, nsaid lesions

Colorectal ca

1. Epidemiology
a. Europeans
b. ↑ incidence in nz
c. Lifetime risk 1/20 by age 75
d. M>F
e. 2nd + 3rd cause of ca death
f. Wide variation betw countries – dietary factors
2. Risk Factors
a. Low physical exercise
b. Smoking
c. Alcohol
3. Protective factors – calcium, vit d, folate, nsaids, aspirin
4. Etiology
a. Adenomas
i. >90% of CRC arise from adenomas
ii. 5% become malignant (transition from adenoma to malignancy over 5-10 yrs)
iii. High risk adenomas – severe dysplasia, villous, >1cm
iv. Adenomas – usu asx, may bleed
b. Genetic Factors
1. 2-3% of CRC
2. 75% risk by age 70
3. Assoc tumors – endometrium, SB, ureter, renal pelvis
4. Modified Amsterdam criteria
a. 3 or more relatives w CRC or an assoc tumour
b. 2 or more affected individuals are 1st degree relatives
c. 2 or more generations involved
d. 1 or more diagnosed <50
5. Germline mutations in mismatch repair genes
6. Mgt – surveillance colonoscopy 2 yearly from age 20-25 (adenoma carcinoma transition accelerated)
ii. FAP
1. 0.5-1% of CRC
2. Mutation – APC gene (AD)
3. Devt of 100-1000s of adenomas
4. Mgt
a. Screening – from age 12-14 with 1-2 yearly sigmoidoscopy
b. Prophylactic colectomy
c. Gastroscopy screening from age 30 for duodenal ca (5%)
iii. Peutz-jeghers syndrome – AD, assoc w circumoral pigmentation + hemartomatous polyps throughout GI tr
iv. Sporadic bowel ca
1. 20% of CRC pts have f.hx
2. 1st degr relative – 2x ↑ risk
3. 2 1st degr relatives – 3x ↑ risk
4. Screening – 5 yearly colonoscopy starting 10 yrs prior to index case
5. Site – 40% rectum, 30% sigmoid, 30% rest of colon
6. Pathology – protuberant, ulcerating or structuring
7. Dukes – A 15% of cases, B 35% of cases, C 50% of cases
5. Presentation
a. Rectal bleeding (distal tumor)
b. ∆ bowel habit (diarrhea or constipation) – esp if L sided
c. Colicky lower abdo pain +/- distension – esp if obstructing
d. Iron deficiency anemia – esp R sided
e. Abdo mass – usu RIF
f. Emergency admission – obstruction, perforation 20%
6. Ixs
a. Sigmoidoscopy
b. Colonoscopy – higher sensitivity for detecting polpys + polypectomy
7. Tx
a. Colon ca
i. Surgical resection (segmental) incl associated mesentery and most prox L/Ns
ii. Dukes C – adjuvant chemo
b. Rectal ca
i. Ant resection and total mesorectal excision (TME aka extrafascial excision) + anastomosis (if propria fascia Ø involv)
ii. Abdomino-perineal resection if sphincter involvement – distal sigmoid, rectum and anus removed
c. Malignant polpys
i. Removal by colonscopic polypectomy
ii. Ø further tx reqd if complete excision + Ø vasc/lymphatic invasion – if doubt → segmental resection
8. Prevention
a. Popn based – dietary change (↓ animal/fat, ↑ high fiber sources, fruit and veges)
b. High risk screening
c. Popn screening of ave risk individuals
i. Faecal occult blood tests
ii. Flexible sigmoidoscopy
iii. Screening colonoscopy ages 50 and 60
iv. Virtual colonoscopy – unable to detect small polyps, ~25% still need colonoscopy to remove polpys, bowel prep and air insufflation still reqd

Esophageal ca

1. Types
a. Squamous cell carcinoma
b. Adenocarcinoma (most common in nz)
2. Epidemiology
a. M:F 3:1
b. ↑ incidence of adenomcarcinoma - ?↑ acid secretion - ?weight gain, ?better nutrition, ?H.pylori eradication
3. Etiology – adenocarcinoma
a. Arise from upgrowth of ca arising in stomach OR
b. Columnar epithelium replaces squamous epith in lower esophagus (barretts esophagus pre-malignant ∆) – acid related
4. Presentation
a. Progressive dysphagia (late)
b. Weight loss
c. Coughing or aspiration (rare, due to tracho-esophageal fistula)
5. Ixs
a. Radiology – detail
b. Endoscopy – biopsy
c. CT +/- Endoscopic US - staging
6. Mgt
a. Surgical resection
i. ~20% only suitable for resection + potential cure
ii. Operative mortality 8-10%
iii. Overall 10-20% 5 yr survival
iv. Adjuvant chemo improves 5 yr survival
b. Dysphagia palliation
i. Mean survival 6 months
ii. Endoscopic intubation - self expanding metal stent
iii. Radiotherapy – SCC more radiosensitive, may heal with strictures requiring stent
iv. Radiotherapy + Chemo – offer cure rates up to 20% (comparable to surgery)

Gastric ca

1. Epidem – M/PI 2-4x ↑ risk, incidence falling in countries adopting a western lifestyle, M:F 2:1
2. Etiology – usu arises in context of chr gastritis (h.pylorif infected individuals at 2-4x ↑ risk)
3. Histology → adenocarcinoma
a. Intestinal cancers (gland forming) – older males, assoc chr gastritis
b. Diffuse gastric cancers – younger M=F pts, genetic factors
4. Presentation
a. Sxs (generally occur too late to consider resection)
i. Early satiety
ii. Weight loss
iii. Anorexia
iv. Vomiting
b. Exmn
i. Epitastric mass
ii. Succession splash from pyloric obstr
iii. L supraclav L/A
5. Mgt
a. Surgical – unsuitable for most pts
b. Chemo may be of benefit
c. Non-operative palliation – pain and dysphagia relief

Abdo Radiology

1. Approach – Gases, Masses, Stones and Bones
2. SBO
a. Identify SB – central, small calibre (<3 cm), valvulae extend across lumen
b. Features of SBO
i. Multiple dilated loops of SB – distension >3cm
ii. Large bowel non-distended
iii. No air in sigmoid/rectum
iv. Air fluid levels on erect
v. Sausages, String of beads sign
c. Presentation – N/V, Øflatus/wind, abdo distension + percussion resonance, tinkling b/s
d. Etiology – adhesions, hernias, volvulus, cancer, gallstone ileus, strictures (crohns, ischemia)
e. Mgt
i. Previous surgery → dx adhesions → surgery
ii. Ø prev surg or atypical pres → CT
3. LBO
a. Identify LB – peripheral, thick haustral folds not extending across lumen, large diameter 5-6 cm, feces present
b. Features of LBO
i. Dilated colon to point of obstruction
ii. Air in LB → dilation (>6cm transverse, >9cm cecum)
iii. Ø air in sigmoid/rectum
iv. Ø air in SB (unless ileocecal valve incompetence causing decompression – LBO starts looking like SBO)
c. Etiology – bowel ca, cecal or sigmoid volvulus, hernia, diveritulitis
d. Complications – risk of cecal perforation
4. Ileus
a. Features
i. Air in sigmoid/rectum (distension)
ii. Multiple distended loops of SB
iii. Air in LB
b. Presentation – absent or hypoactive b/x
c. Etiology – post op, trauma, meds, peritonitis, e/lyte imbalance
5. Free air – due to rupture of a hollow viscus (perforated ulcer, diverticulitis or trauma/instrumentation)
a. Crescent sign (air under diaphragm)
b. Riglers sign (both sides of bowel wall are visible)
6. Calcifications
a. Rim-like – wall of a hollow viscus eg aneurysm, renal cyst
b. Linear/track like – walls of a tube eg ureter, arterial wall
c. Lamellar – formed in lumen of a hollow viscus eg renal stones, gallstones, bladder stones
d. Cloudlike/amorphorous – formed in solid organ or tumor
7. Other
a. Chr pancreatitis – microcalcifications scattered throughout pancreatitis
b. Phleboliths – pelvic v calcifications, normal, well defined, round (renal/ureteral calculi less well defined)
c. AAA – linear calcification
d. Appendicalth – laminar RLQ pearl/bullseye

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