Lower GI surgery Flashcards

1
Q

COLORECTAL CANCER

i) how many cases are there per year in the UK?
ii) what is overall survival?
iii) name four risk factors
iv) give five indications for referral under 2WW
v) what % of people tested under 2WW have malignancy

A

i) 50,000
ii) 60%
iii) male, increasing age, smoking, alcohol, obesity, FH, IBD
iv) over 40 unexplained weight loss, over 50 rectal bleeding, over 60 with iron defic anaemia/change in bowel habit, palpable mass abdo or rectal, positive FOB/FIT test
v) 1.7%

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2
Q

COLON CANCER - TESTING

i) what is the gold standard type of test? name two tests? name two risks
ii) what may be tested in the blood?
iii) name another screening test
iv) give three indications for surgery
v) what is the usual course of management?

A

i) tissue - colonoscopy, flex sigmoidoscopy
- risks = bleeding, perforationm AKI

ii) FBC, LFT, CEA
iii) FIT/FOB
iv) if clinical suspicion is high, abnormal radiology, obstructive symptoms or pending bowel obstruction
v) usually do endoscopy then staging CT scan and MDT

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3
Q

CEA TEST - COLON CANCER

i) what is it?
ii) what may a rising CEA level indicate
iii) after how many weeks does CEA return to normal after tumour removal?
iv) is it specific?

A

i) carcinoembryonic antigen - production should stop at birth
- tumour marker

ii) rising CEA may indicate progression or recurrence of tumour
iii) after 3 weeks
iv) not specific as also raised in smokers, prostate/lung/ovarian cancer, cirrhosis, emphysema

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4
Q

POPULATION SCREENING FOR COLON CANCER

i) between what ages is it done?
ii) what is currently used and what is it being replaced with?
iii) what is the approx uptake? where is this lower?

A

i) between 50-74yrs
ii) use FOB (faecal occult blood test) being replaced with FIT (faecal immunochemical test)
iii) low uptake - 50-60% and lower in socially deprived areas

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5
Q

FOB VS FIT TEST

i) which is the gold standard?
ii) which one needs 3 sep samples from 3 sep bowel movements?
iii) which is most sensitive and can measure how much human blood is present?

A

i) FOB is gold standard currently
ii) FOB
iii) FIT

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6
Q

COLON POLYPS

i) name two types of adenoma that are found? which has the highest proportion of malignancy?
ii) what is the most common type of adenoma?
iii) what increases the chance of a polyp being malignant?
iv) name three treatments for colonic polyps? what may be used for polyps confied to mucosa

A

i) tubular adenoma - 5% malignant
villous adenoma - 30-40% malignant
tubulovillous adenoma - 24% malignant

ii) tubular adenoma is the most commont type
iii) increased size

iv) TEMS (trans anal endoscopic microsurgery)
TAMIS (transanal min invasive surgery)
open/laparo/robot
- endoscopic mucosal resection for polyps confined to mucosa

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7
Q

TYPES OF COLORECTAL OPERATION

i) what is removed in proctocolectomy?
ii) what is removed in high anterior resection?
iii) what is removed in abdominoperineal resection
iv) name four consequences of bowel surgery

A

i) all of the colon and rectum
ii) lower left part of colon and upper part of rectum as well as nearby LNs and surrounding fatty tissue
iii) signmoid, entire rectum and anus are removed - use desc colon to create a permanent stoma (colostomy) - anal area stitched up

iv) infection/bleeding/injury/leak
- bowel function, sexual function, pelvic pain
- lower anterior resection syndrome - inc irritation

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8
Q

COLON CANCER STAGING AND TREATMENT

i) what two staging methods can be used?
ii) name four sites of distant mets
iii) which two treatments are usually used together?
iv) how long are patients under surveillance for after treatment? what does this comprise of? (3)

A

i) TNM and Dukes (ABCD)
ii) liver, lungs, bone, skin
iii) chemo and RT
iv) 5 years - colonoscopy, CT and CEA + clinical review

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9
Q

UC AND CROHNS DISEASE

i) which one affects the colon only?
ii) which is charac by skip lesions?
iii) which always starts distally, is continous and aff mucosa/sub muc only?
iv) which affects full thickness of bowel wall?
v) name two symptoms more linked to UC and two more linekd to crohns

A

i) UC
ii) crohns
iii) UC
iv) crohns

v) UC - pus in stool, fail to defacate, rectal pain, fatigue
crohns - swollen eyes, N+V, mouth sores

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10
Q

UC/CD HISTOPATHOLOGY

i) which has chronic inflam cells?
ii) which is full wall thickness?
iii) which has crypt abscesses and distortion?
iv) which has lymphoid hyperplasia and granulomata?

A

i) both
ii) CD
iii) UC
iv) CD

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11
Q

ACUTE SEVERE UC

i) does smoking make it better or worse?
ii) what may be seen in the stool
iii) what is faecal calprotectin? what is it raised in presence of?
iv) what may be seen in colonoscopy? (3)
v) which criteria can be used to quantify?

A

i) quitting smoking can exacerbate
ii) bloody diarrhoea

iii) neutrophil protein detected in stool whent here is inflamation
- used in young people to look at IBD vs IBS
- not good at detecting cancer but can be a predictor of relapase in IBD

iv) deep ulcers, severe inflamm, blood and purulent exudate
v) truelove and witts criteria

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12
Q

UC MANAGEMENT

i) what must be ruled out?
ii) at what day must there be significant improvement? what happens if there is not?
iii) name the three main treatments used for IBD?
iv) when is surgery escalated to if there has been no improvement? give three indications for this
v) what can be given in frequent flares? what screening must be done 8-10 yrs later

A

i) toxic megacolon - dilated and non viable and susceptible to perforation

ii) need significant improvement at day 3
- if not then need treatment escalation > imaging, immunosupp (ciclosporin) or infliximab, surgical review

i) steroids, aspirin, immunosuppression

iv) day 7 no improvement > surgery
- fuliminant colitis/toxic megacolon, unresponsive to medical therapy, steroid dependence, dysplasia/malignancy

v) azathioprine
- do bowel cancer screening

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13
Q

CROHNS DISEASE

i) what may be seen on colonoscopy?
ii) what other organ needs imaging?
iii) name three complications of CD
iv) name three treatments that can be used?

A

i) rectal inflam, ulceration, granuloma formation ]
ii) small bowel - MRI, pillcam
iii) obstruction, fistula formation, malabs, anaemia

iv) steroids, immunosupp eg cyclosporine, aspirin
(as well as biologics)

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14
Q

COMPLICATIONS OF IBD TREATMENTS

i) what can anti inflammatories eg aspirin worsen?
ii) name four side effects of steroids
iii) name three complications of immunosupressants eg azathioprine
iv) name four complications of biologics

A

i) diarrhoea
ii) weight gain with abnormal distribution, thin skin, osteoporosis, prox myopathy, hypokal, impaired gluc tolerance
iii) myelotox, hepatotox, pancreatitis, GI intol
iv) allergic reactions, local reac to infection, reactivation of latent TB, suscep to opportunistic infecs, cancer such as lymphoma

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15
Q

SURGERY FOR CROHNS DISEASE

i) give four indications for surgery
ii) does extensive resection reduce relapse?
iii) which patients are particularly high risk?

A

i) unresponsive, steroids dependent, dysplasia, strictures/fistulae, terminal ileal disease
ii) no - resect minimal amount possible
iii) patietns on steroids or nutritional compromise

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16
Q

APPENDICITIS

i) who is it common in? who is it rare in? what is it commonly caused by? (3) what causes the inflammation?
ii) what can cause ischaemia? what happens if isch is untreated? name three risk factors
iii) what is the main presenting feature? where does it begin and where does it spread to? what is involved in early and late inflammation?
iv) what is rovsings sign? what is the psoas sign? name three other assoc symptoms
v) where is Mcburneys point? how is it implicated? when may guarding be seen?

A

i) common in young people and children but rare in elderly
- typically caused by direct luminal obstruction - usually due to faecolith (mass of faeces) or lymphoid hyperplasia, impacted stool or a tumour (rare)
- due to obstruc > commensal bacteria can multiply > acute inflam

ii) reduced venous draininage and local inflam can increase pressure in appendix > ischaemia
- if ischaemia is untreated > necrosis of appendicial wall > perforation
- RFs - genetics, caucasian, summer

iii) Abdominal pain is the main feature - initially peri umbillicaal (dull and poorly localised - visc peritoneal inflam)
- then migrates to the R iliac fossa (parietal peritoneum inflam)
- early inflam > appedicial irritation - visc pain not well localised > pain referred to dermatome corresponding to sp cord entry of symp fibres (T10/11)
- late inflam > parietal peritoneal irritation = pain in RIF

iv) Rovsing sign - RIF pain on palpation of LIF
- Psoas sign - RIF pain with extension to R hip (appendix inflam puts psoas major in retrocaecal pos)
- vomiting, anorexia, nausea, diarrhoea, constipation

v) percussion pain over McBurneys point (2/3 way froom umbilucus and ASIS)
- guarding in perforation

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17
Q

APPENDICITIS TX

i) what should be done for all pts to rule out renal/urological cause? what else needs to be ruled out? which two imaging may be done if dx inconclusive?
ii) what is definitive sx tx? what may be done if uncomplicated disease? what should be done for an appendix mass? (2)
iii) name four complications

A

i) urinanalysis for all patients with suspected appendicitis to exclude renal or urological cause
- also do Pregnancy test
- imaging - not essential to diagnose but may order US or CT if inconclusive dx

ii) Definitive treatment is lap appendicetomy - gold standard due to low morbid procedure > send appendix to histopath to look for malignancy
- may use conservative abx therapy in uncomplicated appendicitis but surgery should be standard
- If appendix mass - antibiotic therapy is favoured ith interval appendectomy 6-8 wks later

iii) perforation - if untreated appendix can perforate and cause peritoneal contamination (may happen in children with delayed px)
- surgical site infection
- appendix mass where small bowel and omentum adhere too appendix
- pelvic abscess > confirm on CT > give abx and perc drainage

18
Q

BOWEL OBSTRUCTION

i) what is it? what happens? what are the three types - explain
ii) what is the most common cause of small bowel (2), what is the most common cause of large bowel (3)?
iii) name two intraluminal, mural, extra mural and non mechanical causes
iv) name three symptoms seen? what type of constipation is seen?
v) what may be elicited on examination? what is felt on palpation / if ischaemia is present? what is percussion? what is heard in auscultation?
vi) what cause points to localised and constant pain with perotonism, fever and raised WCC?

A

i) mechanical blockage of bowel where a struc pathology blocks passage of intestinal contents
- occlusion of bowel segment > gross dilatation of prox area > increased peristalsis of bowel > secretion of large vol of electrolyte rich fluid into bowel (third spacing)
- can be simple, closed loop or strangulated
- closed loop = second obstruction proximally eg in volvulus > surgical emergency as bowel will distent and stretch until ischaemiac or perforates
- strangulated > compromised blood supp

ii) most common cause of small bowel = adhesions and hernia
- most common cause of large bowel = malignancy, diverticular disease and volvulus

iii) intraluminal causes - gallstone ileus, ingested foreign body and faecal impaction
- mural causes - cancer, inflam strictures, intusscepton, diverticular stricture, meckeles divertic, lymphoma
- extramural - hernia, adhesion, peritoneal mets, volvulus
- non mech = paralytic ileus - usually small bowel = post op

iv) abdo pain - colicky or cramping (second to perstalsis)
- vomiting - occ early in prox obstruction and late in distal
- abdo distention
- absolute constipation (both flatus and faces)- early in distal and late in prox

v) on exam > evidence of underlying cause eg surgical scar, hernia or abdo distention
- palpate > focal tenderness > guarding or rebound tender if ischaemia
- tympanic on percussion
- tinkling bowel sounds on auscultation

vi) strangulation > looc and constant pain with peritonism, fever and raised WCC

19
Q

BOWEL OBSTRUCTION INVESTIGATIONS AND TX

i) name five bloods that should be done? what WCC is seen? name to things that should be monitored?
ii) what may VBG show? (2) which imaging technique is best to use? what may be seen on AXR in small and large bowel obstruction? what may be seen on CXR in perforation? (3)
iii) what does management depend on? (3) name two things that are given in immed management? which two causes warrant urgent surgery?
iv) what is done in conservative management? name two drugs that can be given? which cause can be initially treated conservatively? what study should be done if case doesnt resolve in 24hrs with conservative mx?
v) which type of cause doesnt usually resolve alone? name two indications for surgery? what surgery will be done?
vi) name three complications

A

i) urgent bloods - FBC, CRP, UE, LFT and group and save
- high WCC, dehydrat, increased amylase if strang/perf
- monitor electrolytes and third space losses

ii) VBG for ischaemia (high lactate) and assess of metabolic derangement
- CT with IV contrast - more sensitive than AXR as can differen between mech and pseudo obstruc and find the site of the case
- plain AXR can still be used - see dilated bowel, >3cm central abdo location and valvilae conniventes (lines across the bowel) if small bowel
- AXR - large bowel = dilated bowel >6cm or caecum >9cm, peripheral location, haustral lines visible
- CXR to look for air under diaphraghm > perforation

iii) management depends on aetiology and whether there is ischaemia, perforation, peritonism
- immed mx - fluid resus as usually intravasc fluid deplete > attention to f luid balance (may need several litres in first 24hrs) and most need a urinary catheter
- closed loop bowel or ischaemia > urgent sx

iv) Conservative if no isch or strangulation > drip and suck
- drip and suck = make patient nil by mouth and insert NG tube to decompress bowel (suck) then start IV fluids to correct electos (drip)
- drugs > analgesia with anti emetics
- adhesional small bowel obstruc should be treated conservatiely initially
- water sol contrast study in cases that dont resolve in 24hrs with cons mx > if contrast doesnt reach colon by 6 hrs then unlikely to resolve > theatre

v) large bowel/small bowel without adhesions usually dont resolve alone
Surgery > always if suspect ischaemia or closed loop obstruc
reasons for sx
- if cause needs surgery eg strangulated hernia or obstruc tumour
- if patient fails to improve with cons mx after 48hrs
- will need laparotomy and may resect bowel and give stoma

vi) bowel ischaemia, bowel perforation > facecal peritonitis, dehydration and renal Impair

20
Q

DIVERTICULAR DISEASE

i) what is a diverticulum? where does it most commonly occur? what is diverticulosis? what is diverticular disease? what is diverticulitis? what is a diverticular bleed?
ii) what % of cases are symptomatic? does it affect M or F more? why does prevalence increase with age? what can form in chronic causes? name four risk factors?
iii) what classification is used? what is this based on?

A

i) diverticulum is outpouching of bowel wall - most common in sigmoid colon
- diverticulosis = pres of diverticula but asymp
- diverticular disease = symptomatic diverticula
- diverticulitis = inflam of diverticula
- diverticular bleed = diverticulum erodes into a vessel > large vol painless bleed

ii) only 25% cases symptomatic and affects men more
- ageing bowel becomes weakned > stool through lymen causes increase in luminal pressure and outpouching of mucosa through weaker areas of bowel
- bacteria can overgrow in outpouchings > diverticulitis > perforate > peritonitis sepsis and death
- fistulae can also form in chronic cases
- RF = age, low fibre, obesity, smoking, FH, NSAID use

iii) stage disease with hinchey classification based on CT findings
- most are asymp and found incidentally

21
Q

DIVERTICULAR DISEASE

I) name three symptoms of DD, AD, perforated diverticulum? which two drugs can mask symptoms of diverticulitis?

ii) what investigation can be done if dx is unclear? what can be done to rule out urological causes?
iii) what does CT abdo pelvis show in diverticulitis (3)
iv) which investigation should never be done? why? what may be done if uncomplicated DD is suspected?

A

i) diverticular disease > intermittent lower abdo pain (colicky), relieved by defacation, altered bowel habit, nausea, flatulence (no systemic features)
- acute diverticulitis > acute abdo pain, sharp, loc in LIF, worse on movement, localised tenderness and systemic upset (low appetite, pyrexia, nausea)
-perforated diverticulum > localised peritonism or general peritonitis > extremly unwell and can be fatal
* corticosteroids/immunosupp can mask symptoms of diverticulitis

ii) fecal calprotectin if dx is unclear (intestinal inflam)
- urine dip to rule out urological causes

iii) CT abdo pelvis - diverticulitis = thickened colonic wall, pericolonic fat stranding, abscess, loc air bubbles, free air

iv) never do colonoscopy due to risk of perf
- if suspected uncomplicated DD then do flexible sigmoidoscopy to ident lesions

22
Q

DIVERTICULAR DISEASE TREATMENT

i) how can uncomplicated DD be managed? (2) what may be done as an outpatient? how should diverticular bleeds be managed initially? what can be done if this doesnt work
ii) name three things that can be given in AD? what can be done if patient deteriorates?
iii) name two indications for surgical management? what procedure will be done? what can be done later?
iv) name three complications

A

i) uncomplicated DD - outpatient mx with simple analgesia and oral fluid intake > may do outpatient colonoscopy to look for masked malignancy
- diverticular bleeds > manage conservate as most are self limiting (signif bleed > resus and blood products)
- if bleeding doesnt respond to conservative mx then may need embolisation or surgical resection

ii) AD > abx, IV fluid, analgesia (symptoms usually improve in 2-3 days) > if deterirotate then repeat imaging to check for progress or complication

iii) sx manage > perforation with faecal peritonitis or overwhelming sepsis
- sx = hartmanns procedure - sigmoid colectomy and end colostomy
- may be able to reverse colostomy and anastomise at later date in 50% cases

iv) diverticular abscess
- diverticular stricture following repeated inflammation > scarred and fibrotic > stricture (need sigmoid colectomy as usually in large bowel)
- fistula formation due to repeated inflam > colovesical fistula (bowel and bladder) and colovaginal fistula (bowel and vagina) > need surgery

23
Q

GI PERFORATION

i) where can it occur? what can happen if there is delay in resus and definitive surgery? (2) name four things that can cause perforation?
ii) name four symptoms? what does perotonism suggest? what is seen in thoracic perforation? (3) what is riglers sign? what is psoas sign?
iii) what is seen on bloods? what is gold standard imaging? name two other imaging techniques that may be used

A

i) can occur any any anatomical location from upper oes to anorectal junction
- delay in resus and defintive sx > septic shock, multi organ dysfunc and death (needs to be ruled out quickly in pts with acute abdo pain)
- caused by diverticulitis, PUD, GI malignancy (gastric/colon), iatrogenic (endo), trauma, foreign bodu, appendicitis, mesenteric ischaemia, obstruction eg cancer or faeces, severe colitis eg CD, excessive vomiting

ii) pain - rapid onset and sharp, systemically unwell and assoc malaise, vomiting and lethargy (may look septic)
- peritonism - loc or generalised (rigid abdo) - generalised implies diffuse contamination of abdo and patient may be very unwell
- thoracic perf = pain, chest/neck/radiating to back and worse on inspiration, assoc vomiting and resp symptoms
- riglers sign - double ‘both sides’ of bowel visible - air in lumen and in peritoneum
- psoas sign - loss of sharp delination of psoas muscle border

iii) see raised WCC and CRP
- gold standard imaging is CT - free air and suggests location of perf
- erect CXR and AXR used to be used for dx but not as spec as CT

24
Q

GI PERFORATION TREATMENT

i) what should be done early? (3) what does further treatment depend on?
ii) which patients may be able to managed conservatively? (3)
iii) what does surgery depend on? what is done in peptic ulcer perforation? what is done in SI perforation? what is done in LI perforation?

A

i) early assessment as resus and broad spec abx, NBM and consider a NG tube
- further txdepends on site of perf and patient factors - most require surgical repair and control of contaimination
- identify caue > manage perf > thorough washout
ii) some pts can be managed conservatively eg localised diverticular perf - localised peritonitis and tenderness with no evidence of general contam on imaging
- pts with sealed upper GI perf / without general peritonism
- elderly/frail patients with lots of co morbids who would be unlikely to survive sx

iii) dep on pathology and location
- peptic ulcer perf - upper midline insicision and patch of omentum is tacked over the ulcer (graham patch)
- small bowel perf - midline lap - over sew if bowel is viable but if non viable > bowel resection and stoma
- large bowel perf - midline lap - resection with stoma formation if faecal contamination

25
Q

HAEMORRHOIDS

i) what are they? what are they made of? what are they classified according to? name three risk factors?
ii) what is the most common symptom? name four other symptoms? how may a prolapsed haemmorhoid appear? when may exam not be normal?
iii) what investigation is done to confirm diagnosis? what should be done if there is a complication to exclude other pathology?

A

i) abnormal swelling or enalargement of anal vascular cushions ( act to assist anal sphincter in maintaining continence)
- three vasc cushions pos at 3,7,11 oclock when looked at patient in lithotomy position
- cushions can become abnormally enalarged > pathological
- classified according to size - 1st degree (remain in rectum) to 4th degree (persistently prolapsed)
- RF - excess straining from chronic constipation, increased age, raised intra abdo pressure (preg, chronic cough, ascites)

ii) painless bright red rectal bleeding - commonly after defacation on paper or in toilet (blood is seen on surface of stool, not mixed in)
- also get itching due to chronic mucus discharge and irritation, anal lump, rectal fullness and soiling due to in incontinence
- large prolapsed haemm can thrombose > painful > purple/blue/oedematous/tense/tender perianal mass
- exam usually normal unless they have prolapsed

iii) proctoscopy (rigid sigmoidoscopy) to confirm dx
- significant bleeding > FBC and clotting screen
- colonoscopy if complication to exclude other anal pathology

26
Q

HAEMORRHOIDS MX

i) how are most managed? name three lifestyle advice that may be given? anme two drugs that can be given
ii) how can 1st and 2nd degree be treated? how may 2nd or 3rd degree be treated? what is done for 3rd/4th degree?
iii) name three post op complications

A

i) most are managed conservatively espec if uncomplicated
- lifestyle advice > increase fibre and fluids to decrease constipation
* laxatives and topical analgesia eg lidocaine gell or oral opioids if symptoms worsen

ii) 1st and 2nd degree can be treated with rubber band ligation > draw haemm into suction fun and place rubber band over the next (in clinic or theatre)
Surgical mx
- haemmorhoid artery ligation for 2nd or 3rd degree > identify with doppler then tie it off > infarcts and falls off
- haemmorhoidectomy for 3rd and 4th dergree > excise tissue ensuring internal sphincter muscle reamins

iii) Post op = recurrence, stricturing, faecal incontinence

27
Q

ANAL FISSURE

i) what is it? what is it most commonly due to? what classes it as acute or chronic? what is primary and secondary? name three RFs
ii) name four symptoms? what may be felt on DRE? where do most present? what may be needed if in lots of pain?
iii) what imaging technique identifies them? do most patients need surgery?
iv) name two lifestyle changes? name three drugs that can be given initially? what is given if pt is still symptomatic (2) how do these work?
v) who is surgery reserved for? name two things that can be done? name a complication

A

i) tear in the mucosal lining of the anal canal most commonly due to trauma from defacation of hard stool
- acute - present for <6 weeks or chronic - present for >6 weeks
- primary = no underlying disease or secondary (underlying difease eg IBD)
- RF are constipation, dehydration, IBD, chronic diarrhoea

ii) intense pain post defacation - can last several hours (pain disproportionate to size of fissure), bleeding, itching post defacation
- on exam fissure can be visible/palpable on DRE
- most present in posterior midline (anterior more common in females)
- may need to do DRE under anaesthesia as so painful

iii) identify by protoscopy (rigid sigmoidoscopy)
- most patients dont need surgery

iv) medical mx > reduce risk factors and give adequate analgesia
* increase fibre and fluid intake
* stool softening laxatives eg movicol or lactulose and topical anaesthetics > lidocaine for short term symptom relief
- if still symp > give GTN cream or diltiazem cream > increases blood supply to region and relaxes internal anal sphincter > less pressure > promotes healing

v) surgery reserved for chronic fissues where medical mx fails after 8 weeks
* botox injections to internal anal sphincter to relax and promote healing
* lateral spincterectomy > divison of internal anal sphinc muscles
- complication > recurrence

28
Q

ANAL FISTULA

i) what is it? what are most associated with? what classification system is used? what are the four different types?
ii) what is the typical RF? name three other RFs? how do patients usually present? (3) what may be seen one exam? what may be felt?
iii) what rule can be used to predict clinical trajectory? which imaging should be used to visualise tract and plan surgery? what does definitive mx depend on?
iv) what is done for superficial disease? what does this lead to? what can also be done to bring the fistula together and close the tract? is there any difference in outcomes for different sx approaches?

A

i) abnormal connection between anal canal and perianal skin
- most are associated with anorectal abscess formation
- Parks classification system > four types = inter sphincteric fistula (most common), trans sphincteric, supra sphincteric (least common) and extra sphincteric

ii) perianal abscess if typical RF however also IBD eg crohns, systemic disease eg DM, trauma to anal region, previous RT to anal region
- usually present with reccurent peri anal abscesses or intermittent/continuous discharge onto perineum inc mucus, blood, pus, faeces
- on exam > external opening on the perineum may be seen - can be open or covered in granulation tissue
- may feel a fibrous tract underneath the skin on DRE

iii) Goosall rule can be used clinically to predict trajectory of fistula dep on location of external opening
- MRI to visualise anatomy of tract and plan sx management
- definitive management depends on cause and site

iv) fistulotomy (superficial disease) = lay tract open by cutting through skina nd subcut tissue > heal by secondary intention
- placement of a seton through the fistula attempts to bring it together and close the tract
- no difference in outcomes for differenti interventions but decided on the course of the tract

29
Q

ACUTE MESENTERIC ISCHAEMIA

i) what is it? name four causes and what causes each? name three RFs?
ii) what type of abdo pain is felt? what can it be associated with? what is seen in later stages? what should be looked for to find underlying cause?
iii) what investigation needs to be done urgently? what blood marker may be high? how may LFTs be affected? what is definitive imaging for diagnosis? how will arterial ischaemia show on imaging? (2)
iv) name four things that should be done in imminediate treatment? which department should be contacted? what is done surgically for definitive mx?
v) what will many patients end up with post operatively? what may be able to be done? name two complications? what is mortality rate?

A

i) sudden decrease in blood supply to the bowel > death if not promptly treated
Causes: thrombus in situ (mesenteric arterial thrombosis) > atherosclerosis
- embolism > cardiac causes/thoracoabdo aneurysm
-non occlusive cause > hypovol/cardiogenic shock
-venous occlusion and congestion >coagulopathy, malig, autoimmune - RFs dep on underlying cause - for embolism = smoking, hyperlipid, HTN

ii) generalised abdo pain out of proportion with clinical findings, diffuse and constant pain associated with nausea and vomiting
- non specific tenderness OE abdo with no spec signs
- in later stages > global peritonism
- look for embolic sources eg AF to suggest underlying cause

iii) ABG urgently - look for acidosis and serum lactate > severity of infarction
- routine bloods - FBC UE clotting, amylase (rises in mesen isch) and LFT (liver derange if coeliac trunk is aff)
- definitive dx requires CT with IV contrast - triple phase with thin slices in arterial phase
- arterial isch will show as oedematous bowel on CT initially then loss of bowel wall enhace then pneumatosis (gas in wall of intestine)

iv) Surgical emergency that requires immed resus
- IV fluid, catheter, fluid balance chart, broad spec abx to decrease risk of faecal contam in case of perforation
- early ITU input as patient will be acidotic and high risk of multi organ fail
Definitive mx: excision of necrotic or non viable bowel if not suited to revasc - post op ITU and relook laparotomy in 24-48hrs

v) many patients will end up with stoma
- may be able to revasc the bowel - remove thrombus/embolism radiologically (pref to be done through angio due to risk of aortic contam inopen surgery)
- bowel necrosis and perforation
- short gut syndrome > malabs due to lack of functional small intestine
- mortality is 50-80%

30
Q

CHRONIC MESENTERIC ISCHAEMIA

i) what is it? what three vessels are implicated? what age and sex is more common? what causes it? how many vessels must be implicated - why?
ii) what causes exacerbation of symptoms? name three RFs? why are lots of patients asymp? name three symptoms? what is found on examination? (3)
iii) will bloods routinely be normal or abnormal? what electrolyte should be checked? what risk factor profile should be done? what is dx imaging of choice?
iv) what lifestyle advice should be offered? name two medical therapies that should be started? which two surgical approaches can be taken? what is preferred?
v) name two indications for surgery? name a procedure for each approach? name two complications? is prognosis good?

A

i) reduced blood supply to the bowel that gradually deteriorates over time as a result of athero in coeliac trunk, SMA or IMA
- >60yrs and more common in females
- gradual bup of athero plaque > narrows lumen and impairs blood flow to viscera > inadequate supply to bowel
- at least two of coeliac SMA or IMA must be affected to be symptomatic due to collateralisation (one vessel will likely be completely occluded)

ii) increased demand on blood supp eg eating, reduction in blood vol eg haemmorhage will exacerbate symptoms
- RF - smoking, HTN, DM, hypercholesterol
- often asymp due to collateralisation of mesenteric vessels (asymp at rest but symptomatic when increased demand)
- post prandial pain (10min-4hrs post eating), weight loss - decrease calorie intake and malabs, may get change in bowels (loose), nausea, vomiting
- exam findings often non spec > malnut and cachexic, general abdo pain, abdo bruit

iii) bloods will routinely be normal
- check magnesium (malnourish)
- CV risk factor profile
- CT angio is imaging dx test of choice . Good anatomical view of all vessels

iv) modify RFs espec smoking
- start anti plat and statin therapy to minimised progression
- can do endovasc or open surgery (endovasc is preffered - managed by IR and vascular surgeons)

v) surgery if severe/progressive disease or debilitating symptoms eg weight loss/malabs
- endovasc = mesenteric angioplasty (balloon to dilate vessel) with stenting
- open = endartectomy or bypass procedure
bowel infarction
- malabsorption
- prognosis is good and results from endovasc and open surgery are comparable

31
Q

IRRITABLE BOWEL SYNDROME

i) what is it? what is it associated with? who is it most common in? what criteria is used for diagnosis?
ii) name three things that a 6 month history of can point towards IBS? name three red flag symptoms that should not be missed?
iii) name three lifestyle changes that can be implemented? name three pharma drugs that can be trialled? if patient is refractory to tx - what can be done?

A

i) * functional bowel disorder > abdo pain and discomfort is assoc with defacation and/or change in bowel habit in absence of organic cause
- more common in women 20-30yrs
- altered GI sensitivity towards stimuli > may be triggered by enviro factors (physiol and psych stress) and foods/bacteria
- Rome criteria for diagnosis

ii) 6 months hx of: abdo pain/discomfort. bloating, change in bowel habit
Must elicit red flag features
- unintended weight loss
* rectal mass/bleeding
* FH bowel or ovarian cancer
* aged over 60 with >6weeks altered bowel habit

iii) diet change - regular meals and adequate hydration - avoid high fibre, starch, caffiene, carbonated drinks
- Single avoidance diet - low FODMAP
- pharma therapy - anti spasmodics, laxatives or anti motlility (loperamide), amytriptyline
* consider psych therapy - CBT, psychotherapy, hypnotherapy if refractory to other tx

32
Q

RECTAL PROLAPSE

i) what is it? who does it mainly affect? what happens in partial and full thicness prolapse? what causes each? name four risk factors
ii) name four symptoms? which type may present with rectal fullness, tenesmus or repeated defacation? what may the patient have to do to elicit results on examination? what may be found on DRE?
iii) name an imaging investigation that is used in internal prolapse? name three groups that may get conservative mx? what dietary changes can be made? what can be done for a minor mucosal prolapse?
iv) what is the only definitive mx? name two surgical approaches that can be taken? which approach is preferred in elderly?

A

i) protrusion of mucosal/full thickness layer of rectal tissue out of the anus
- mainly affects older females
* partial thickness - rectal mucosa protrudes out of anus
* full thickness - rectal wall protrudes out of anus
* full thickness is a form of sliding hernia through a defect in fascia in pelvic region
* may be caused by chronic straining/constipation, chronic cough or multiple vaginal deliveries
* partial thickness > assoc with loosening and stretching of connective tissue that att rectal muc to rectal wall >often occ with haemmorhoids
* RF = increasing age, female, multiple deliveries, straining, anorexia

ii) rectal mucus and discharge, faecal incontinence , PR bleeding, visible ulceration
- full thickness being internally and can present with sensation of rectal fullness, tenesmus or repeated defacation
- may not be obv on exam > ask patient to strain
- DRE > weakened anal sphincter

iii) defacating proctography and exam under anaes for internal proalpse
- conservative mx is more common if unfit for sx, minimal symptoms or in children
- increase dietary fibre and fluid intake
* minor mucosal prolapse may be banded in clinic
* surgical is only definitive mx: perineal approach - delormes and altermeiers operation
* abdo approach - laparascopic, robotic or open > rectum is mobilised and fixed onto sacral prominence via suttures or mesh
* no difference in post op outcomes between procedures
* perineal are preferred in elderly as safer

33
Q

VOLVULUS

i) what is it? what can happen to the affected bowel? where does it most commonly occur? why? name four RFs?
ii) how does it present? name three earlier signs and one late sign? is onset slow or quick? what is percussion? what does peritonism indicate?
iii) which bloods need to be done to exclude a pseudoobstruc (3)? what initial imaging is done - what does this allow identification of? what is classically seen on imaging? what may AXR show?
iv) how are most treated? (2) how do each of these work? what surgical approach is usually taken? give four indications for this
v) name three things decision to operate depends on? name two complications? what is risk of recurrence?

A

i) twisting of a loop of intestine around mesenteric attachment > closed loop bowel obstruc
- affected bowel can become ischaemic due to compromised blood supp > necrosis and perforation
- most occur at sigmoid colon > common cause of large bowel obstruction (long mesentery of sigmoid means segment is more prone to twisting on its mesenteric base > volvulus)
- RFs - increasing age, neuropsych disorders, nursing home resident, chronic constipation/laxative use, male gender, prev abdo operation

ii) present with clinical features of bowel obstruction
- sigmoid is distal to GI tract > vomiting is a late sign
* colicky pain, abdo distention, absolute constipation are earlier signs
* volvulus has rapid onset (few hrs) and lots of abdo distention (compared to other causes of bowel obstruc)
* OE - abdo is tympanic to percussion
* peritonism indicates ischaemia or perforation > sx emergency

iii) electrolytes, Calcium, TFTs to exclude pseudo obstruc
- initial investigation is CT abdo pelvis with contrast > ident site and cause > classically see dilated sigmoid colon with ‘whirl sign’ twisting mesentery around the base
- may do AXR > show coffee bean sign from lefy iliac fossa (if ileocaecal valve is incompetent then AXR also shows small bowel dilatation)

iv) most are treated conservatively with decompress by sigmoidscope and insertion of flatus tube
- sigmoidscope decompress > patient in left lateral post and scope > twisted bowel > relieve obstruction = rush of air and liquid faeces
- flatus tube left in situ for up to 24hrs to allow for continued passage of contents
- Surgical mx > usually laparatomy for hartmanns (rectosignmoid stump with end colostomy)
- indicated if colon isch or perf, repeated failed attempts at decompress, necrotic bowel on endoscopy

v) decision to op dep on nutritional status, blood supply, haemodynamic stability and pres of perf/peritonitis
complications:
* bowel ischaemia and perforation
* long term > risk of recurrence in 90% pts
* complications from stoma
* mortality from surgery is high

34
Q

RECTAL BLEEDING

i) what is it generally caused by? name four causes? which is the most common cause? what score is used - what does it determine? name four RF for adverse outcomes?
ii) what two groups should patients be stratified into? name three assoc symptoms? what exam is essential? do acute bleeds always initially show drop in Hb?
iii) what should be done to rule out infective cause? what imaging should be done if unstable? what should be done if stable?
iv) what % settle spontaneously? what should be done if unstable (2)? at what Hb should patient be transfused? name three things that can be done in endoscopic haemostasis?
v) what can be done if bleeding point is ident on angiogram? when may surgery be considered?

A

i) generally caused by bleeding from lower GI tract but can occ in upper GI bleed/small bowel lesions
- source from rectum or colon
- pt with large fresh rectal bleed who is haemodyam unstable consider a upper GI bleed unless proven otherwise
* lower GI - diverticular disease, ischaemic/infective colitis, haemmorhoids, malignancy, angiodysplas, CD, UC
* diverticulosis - most common cause LGI bleeding
* oakland score > stratify patients to det if outpt mx is feasible
* RF for adverse outcomes = haemodynamic instab, ogoing bleeding, age >60yrs, serum creat >150, signif comorbids

ii) Stratify into stable to unstable
* nature of bleed - duration, freq, colour, relation to stool
* assoc symp - pain, haematemesis, PR mucus
* PR exam is essential
* acute bleeds may not initially show with reduced Hb

iii) stool culture to exclude infective cause
- unstable - urgent CT angiogram > identify source of bleeding / -
- stable > flexi sigmoidoscopy or colonoscopy to exclude left colonic pathology
- stable with PR and no aborm on colonoscopy > OGD to look for other couces of bleeding

iv) 95% settle spontaneously
- unstable > urgeny resus with AE approach and IV fluid/blood
- Hb <70 > transfuse packed red cells
- reverse anti coag urgently if low Hb
- endoscopic haemostasis methods eg injection of adrenaline, thermal devices or mech therapy eg endoscopic clips and band ligation

v) arterial embolisation if bleeding point is identified on angiogram
- surgery is rarely required but may be consdered in ongoing lower GI bleed with instability or req lots of transdusions where endoscopic and radiol tx has failed

35
Q

CAECAL VOLVULUS

i) which two age groups does it commonly affect? what may cause it in each age grop?
ii) which imaging is used to diagnose? what may be seen
iii) how is it treated? (2)

A

i) second most common type > 10-29 years then 60-79yrs
- younger group may have intestinal malform or excessive exercise
- older group more assoc with chronic constipation/distal obstruc/dementia

ii) dx on CT imaging > distended caecum.mesenteric swirl and small bowel obstruc
iii) tx with laparotomy and ileocaecal resection

36
Q

INGUINAL HERNIA

i) what is a hernia? when does it occur? what are the two main types of ing hernia? what happens in each? how are the two types distinguished?
ii) name three RF for IH? borders of the inguinal canal - what lays anterior, floor, posterior wall and roof?
iii) what is the most common presenting symptom? what symptoms are seen if it becomes incarcerated (trapped) (3)? what may patient present with features of? why?
iv) where is a inguinal hernia located compared to a femoral hernia? how can you distinguish between a direct and indirect hernia on examination?
v) what type of diagnosis is usually done? when would imaging be done? what is first line imaging? what imaging is done if there is obstruc or strangulation?

A

i) hernia > protrusion of part or whole organ/tissue through wall of the cavity that contains it
* occurs when abdo cavity contents enter into the inguinal canal
* most common type of hernia
* two main types - direct (20%) - bowel enters ing canal directly through weakness in posterior wall of canal (hesselbachs triangle) > more common in older pts, second to abdo wall laxity or signif increase in intra abdo pressure
* indirect (80%) - bowel enters ing canal via deep ing ring > arise from incomplete cloure of proces vafinalis (outpouching of peritoneium allowing for testic descent)
* differeniate two types at surgery by identiying the inferior epigastric vessels > indirect will be lateral to vessels but direct will be medial

ii) RF - male, increasing age, raised intra abdo pressure (chronic cough, heavy lifiting, chronic constipation), obesity
* borders of ingunal canal - ant wall = apneurosis of ext oblique, floor - ing lig, post wall = transversalis fascia, roof = int oblique and tv abdominis

iii) most common presenting symptom is lump in groin which initially disappears with minumal pressure or when pt lays down > mild to mod discomofrt on activity or standing
- if it becomes incarcerated > painful, tender and erythematous
- pt may present with features of bowel obstruction if lumen becomes blocked or with features of strangulation if blood supp becomes compromised

iv) ing is supmedial to pubic tubercle, femoral os inf lat to pubic tubercle

reducible on laying down, min pressure
* if it enters the scrotum can you get above it/is it dep from testes
- Differen of direct and indirect hernia > reduce hernia and place pressure over deep ing ring (mid point of ing lig) > ask patient to cough
* if hernia protrude depite occlusion of deep ing ring = direct
* if hernia doesnt protrude = indrect
* assess may be unreliable >only definite way to different is at surgery

v) Typically a clinical dx
* imaging should only be done if there is dx uncertainty or to exclude another pathology
* US is first line if imaging is done
* if features of obstruc or strangulation > CT

37
Q

INGUINAL HERNIA TREATMENT

i) what should be done if symptomatic? what is a feature of strangulation? what needs to be done in this situation? how can an asymptomatic hernia be managed?
ii) what two surgical approaches can be taken? what are preferred to be used in primary (congenital) inguinal hernias? when is laparoscopic surgery done? (4)
iii) what does it mean if hernia is irreducible or incarcerated? what can this show features of clinically? what is the patient at risk of in strangulation?
iv) name three complications of IH? name four post op complications? what do 30% of patients sufer with after surgery? damage to which two vessels can lead to ischaemic orchitis?

A

i) If symptomatic > offer surgical intervention
* if symptoms of strangulation (pain out of proportion to clinical features or deranged biochem) > urgent sx exploration
* no symptoms > can mx conservatively

ii) Surgery > can be repaired open or laparoscopically
* open mesh repairs (support surr tissue as it heals) are prefered if primary ing hernia
* laparoscopic > if bilateral or recurrent hernias (also onsidered in puts with primary unilateral hernia, at risk of chronic pain or in females)

iii) if irreducible or incarcerated - contents are unable to return to orig cavity, obsstruction of bowel lumen > clin features of bowel obstruc or strangulation (compress of hernia has compromised blood supp > bowel is ischaemic)
* strangulated is sx emergency due to time dep risk of bowel infarction

iv) incarceration, strangulation, obstruction
* post op complicatins > pain, bruising, haematoma, infection, urine retention
* recurrence is 1% within 5 years of sx
* chronic pain can occ in up to 30% pts
* damage to vas deferens or testicular vessels > isch orchitis

38
Q

FEMORAL HERNIA

i) is it common? what is there a high risk of? when does it occur? does it affect men or women more? why? name three RFs
ii) what is the femoral canal? what makes up the superior border, anterior border, posterior border, lateral and medial border?
iii) how may a patient present? how will 30% patients present? what needs to be done to determine which hernia type is present? who may this be difficult in? how may the femoral ring appear?
iv) do all patients need surgery? which imaging is usally done? what is done if double in dx or complications?

A

i) uncommon but high risk of strangulation
* occur when abdo viscera or omentum pass through the femoral ring into the potential space of the femoral canal
* more common in women tham men because of wider anatomy of female bony pelvis

ii) femoral canal = anatomical compartment in anterior thigh > sup border is femoral ring, ant border is ing lig, post border is pectineus, lateral border is femoral vein, medial border is lacunar ligament
- RF = female, pregnancy, raised intra abdo pressure, increasing age

iii) small lump in groin
* are usually asymptomatic > 30% will present as an emergency (obstruc or strangulation)
* identify exact location of lump to decide which type of hernia is present > can be difficult in obese patients
* tight femoral ring > unlkely to be reducible (flattens when you lay down or push against it)

iv) need sx intervention
* clinical dx but often also do imaging
* US but operator dep and high index of suspic is needed
* CT abdo pelvis
* if signic doubt in dx or complications > surgically explore

39
Q

FEMORAL HERNIA TREATMENT

i) within what time period should all patients be managed surgically? why?
ii) what is the low approach? what is the high approach? what will surgery aim to do (2)
iii) what increases the risk of strangulation? what other complication may happen?

A

i) all should be managed surgically within 2 wks ofpresentatuon due to high risk of strangulation

ii) low approach > incision below ing lig (doesn’t interfere with ing structures but reuslts in limited space for removal of any compromised bowel)
* high approach > incision above ing lig > preferred in emergency due to easy access of comprommised bowel
* surgery will reduce the hernia and narrow the femoral ring with sutures between pectineal and ing lig or with a mesh plug

iii) strangulation > risk increases with time following initial dx > 3 months its 22% but 21 months its 45%
* risk of obstruction

40
Q

ANORECTAL ABSCESS

i) what is it? is it more common in men or women? what do 1/3 patients have at presentation? what causes it? name three causative organisms?
ii) what will patients present with? what makes it worse? name four systemic featurs that may be seen when severe? what may be seen one exam? (3) how may deeper abscesses appear?
iii) what intervention do most patients need? what test should be sent if they dont have an assoc fistula or rectal pathology? what should be done if atypical presentation?
iv) name two things that should be started once diagnosed? what is main management? (2) how may the wound be left?
v) what procedure can be used to check for a fistula? what may reduce the risk of fistula formation?

A

i) collection of pus in anal or rectal region
* more common in men than women and have high rates of recurrence
* 1/3 have associated perianal fistula at time of presentation
* caused by plugging of anal ducts which drain anal glands in the anal wall > blockage = fluid stasis > infection
* common causative organisms = ecoli, bacteriodes, enterococcus

ii) severe pain in perianal region, worse with direct pressure (when sat down)
* perianal discharge or bleeding
* severe > may present with systemic features eg fever, rigor, malaise, clinical features of sepsis
* OE - erythematous fluctant tender peri anal mass > may be discharging pus/surr erythema
* deeper abscesses may not have obv external signs > severe tender OE

iii) dx is generally clinical
* majority need sx intervention > FBC, UE, clotting G&S
* abscess withput any fistula or rectal pathology > send HbA1C to check for underlying diabetes
* if atypical presentation > additional imaging eg MRI pelvis

iv) start on abx and analgesia
* main mx is exam under anaes rectum with incision and drainage > always under GA
* can be left to heal by secondary intention (left open) with or without packing

v) intra op proctoscopy to check for fistula
* post op abx may lower the risk of fistula formation