Lower GI surgery Flashcards
(40 cards)
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
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%
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?
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
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?
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
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?
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
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?
i) FOB is gold standard currently
ii) FOB
iii) FIT
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
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
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
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
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)
i) TNM and Dukes (ABCD)
ii) liver, lungs, bone, skin
iii) chemo and RT
iv) 5 years - colonoscopy, CT and CEA + clinical review
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
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
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?
i) both
ii) CD
iii) UC
iv) CD
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?
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
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
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
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?
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)
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
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
SURGERY FOR CROHNS DISEASE
i) give four indications for surgery
ii) does extensive resection reduce relapse?
iii) which patients are particularly high risk?
i) unresponsive, steroids dependent, dysplasia, strictures/fistulae, terminal ileal disease
ii) no - resect minimal amount possible
iii) patietns on steroids or nutritional compromise
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?
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
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
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
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?
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
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
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
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?
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
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?
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
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
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
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
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
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?
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