Upper GI surgery Flashcards
ACUTE PANCREATITIS
i) what happens? where would pain be expected? how quick onset? does it radiate?
ii) name three other differentials
iii) name three imaging tests that may be needed
iv) which blood marker would be expected to be very raised
v) what are the two main causes that lead to 80% of AP? what are the other causes? (GET SMASHED)
vi) what is cullens sign? what is grey turner sign?
i) pancreas own enzymes get activated > autodigestion > inflamm and haemmorhage
- sudden onset epigastric pain that radiates to the back
ii) peptic ulcer disease, acute cholecytitis, gastritis/GORD
iii) erect CXR, USS, CT
iv) serum amylase
v) 80% due to gallstones or alcohol excess
Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion venom, ERCP, Drugs
- as well as hyperlipid, hypothermia, hypocalc
vi) cullen = bruising around umbilicus
grey turner - bruising at flanks > retroperitoneal haemmorhage
ACUTE PANCREATITIS
i) what is the modified glasgow score?
ii) what does a score of 3 or more within 45hrs onset mean? what do these patients need?
iii) what is the risk of mortality of patients with a score of 3
iv) how should all patients be managed? what is the mainstay of tx?
v) name five complications of AP
i) predictor of severity of AP
ii) score 3 or more = severe
- need treatment in HDU or ITU
iii) 10-50% mortality
iv) ABCDE approach
- tx mainstay is supportive - treat UL cause, gfluids, catheter, opioids, broad spec abx if confirmed panc necrosis
v) hypovolaemic shock, haemmorhagic pancreatitis, pseudocyst formation ( pressure effect), necrosis, ARDS, chronic pancreatitis
PEPTIC ULCER DISEASE
i) which area of the abdomen is pain expected? name three other symptoms? what is rebound tenderness? what does it indicate? name three other differentials
ii) where are the two most common places for them to occur? which ones present earlier? name four risk factors?
iii) name two things that normally protect the gastric mucosa? what happens in PUD? what two things most commonly cause the damage in PUD?
i) epigastric/retrosternal pain
- nausea, bloating, post prandial discomfort, early satiety
- rebound tenderness - pain on removal of pressure rather than addition of pressure > indicates peritonitis
- acute pancreatitis, bowel perforation, AAA, bowel ischaemia
ii) can occ anywhere in GI tract but are most often located on the lesser curvature of proximal stomach or first part of duodenum
- duodenal ulcers present earlier
- RFs- NSAIDs and H pylori > then corticosteroid use, prev gastric bypass surgery, pshysiol stress eg burns or head trauma or zollinger ellison syndrome
iii) normal gastric mucosa is protected by surface mucus secretion and HCO3- release > PUD - imbalance between protective facotrs
- most common damage is from H pylori or NSAID use
PEPTIC ULCER DISEASE INVESTIGATIONS
i) when is an urgent OGD indicated? do most patients require this? name three ways to test for H pylori?
ii) name five bloods and two imaging tests that should be done
iii) what does air under diaphragm on CT indicate?
i) urgent OGD (most patients dont require this) if new onset dysphagia ir age >55yrs with WL, upper abdo pain, reflux, dyspepsia or new onset dyspep not responding to PPIs
- non invasive h pylori testing > carbon 13 urea breath test, serum antibodies to HP or stool antigen test
ii) FBC, UE, LFT, amylase, CRP, coag screen
- imaging = erect CXR and CT
iii) sign of perforation (gas outside cavity that it should be in)
PEPTIC ULCER DISEASE
i) name three conservative management? what should be avoided? how long should PPIs be given for initially? what should be given if patient has H pylori?
ii) is surgical management common? name three indications for surgery and two procdures that may be done?
iii) name two main complications and what needs to be done for each
iv) name a syndrome where the patient is at increased risk of PUD
i) lifestyle advice > smoking cessation, weight loss, reduced ETOH
- avoid/stop NSAIDs if possible
- PPI therapy for 4-8 weeks to reduce acid prod > reassess
- Hyplori > start on triple therapy = PPI, oral amox/clarith or metranidazole for 7 days
ii) sx management is rare except in emergency eg perforation or in management of zolinger ellison or in severe or relapsing disease > partial gastrectomy or selective vagotom
iii) perforation = surgical emergency (erosion through mucosa into the peritoneal cavity) > laparotomy
- severe haematemesis = surgical emergency (erosion into a vessel internally) may do endoscopy or laparotomy if it fails > put in clips, give adrenaline and cauterise vessel
iv) zollinger ellison syndrome > digestive disorder that results in excess gastric acid secretion
ACUTE CHOLECYSTITIS
i) where would pain be expected to be felt? sudden or gradual onset? associated with?
ii) what may make the pain worse?
iii) what sign may be positive? explain
iv) name three other differentials
v) name three imaging tests that may be ordered?
i) right upper quadrant
- sudden onset > radiates to back
- associated with nausea and vomiting
ii) coughing/movement
iii) murphys sign - get patient to take a deep breath and hold while palpating the right subcostal area > if pain on insp when inflamed gall bladder touches hand = positive murphys sign
iv) ascending cholangitis, pancreatitis, renal colic, appendicitis
v) erect CXR, USS, CT
ACUTE CHOLECYSTITIS
i) what can cause it? (3)
ii) name a common causative organism
iii) if the patient is clinically well - which treatment can be given?
iv) name three complications? what is mirizzi syndrome? what is bouveret syndrome?
i) sludge/stone impaction in GB neck or cystic duct, bile stasis
ii) E coli
iii) send home on oral abx
iv) empyema (GB filled with pus > sepsis > lap chole), GB perforation, gall stone ileus (GS erodes into small bowel causing blockage), pancreatitis, chronic cholecystitis (persistent inflam of GB wall)
- mirizzi syndrome > stone in hartmann pouch or cystic duct > compression of common hep duct > obstrucive jaundice (MRCP and lap chole)
- bouveret - cholecytosduodenal fistula (fistula between GB and small bowel > stone passes into small bowel > get bouv syndrome (stone impacts prox duo and causes gastric outlet obstruc)
GALLSTONES
i) what is the gold standard imaging test?
ii) what are the RFs? (4Fs)
iii) name two types of stone?
iv) what is usually the cause? what do they lead to?
i) USS
ii) female, fat, fertile, forty
iii) cholesterol stones, mixed stones, pigment stones
iv) usually from bile stasis > lead to cholecysitis as gallstone irriate the bladder wall
ASCENDING CHOLANGITIS
i) what is it? what is it usually caused by?
ii) what is charcots triad? what is reynolds pentad?
iii) name four causes
iv) what is seen on US? what is seen on ERCP?
v) what immediate tx should be given? name three things done in definitive mx
i) inflam/infection of the bile duct
- usually caused by ascending bacteria from the duodenum
ii) CT - RUQ pain, jaundice, pyrexia
RP - RUQ, jaundice pyrexia, shock, confusion
iii) gallstones, strictures, malignancy, iatrogenic eg ERCP
iv) US - bile duct dilatation, ERCP - see obstruction
v) immediate - IV broad spec abx for 4-7 days > do cultures, IV access, analgesia
definitive - endoscopic biliary decompress (remove blockage by ERCP)
- perc transhepatic cholangioraphy if patient cant have ERCP
- may do lap chole if gallstones are the cause
BILIARY COLIC
i) what is it?
ii) when does it happen? what can trigger it?
iii) will the patient be systemically well or unwell? what are the 5 RFs
iv) what will be seen on LFT? what imaging should bed one? what is gold standard imaging?
v) which two conservative management should be done? what should be done within 6 weeks of presentation?
i) acute gall bladder pain
ii) happens when a GS transiently blocks the cystic duct and GB contracts
- can be triggered by fatty food
iii) patients are usually systemically well
- fat, female, forty, fertile, family hx
iv) LFT = raised ALP but normal ALT and bilirubin
- trans abdo US - look for sludge, thick GB wall or duct dilation
v) conservative - pain relief, lifestyle mod (low fat diet)
- high change of recurrence so do elective lap chole within 6 weeks
DYSPHAGIA
i) what are the five key questions to ask?
1) is it difficult to swallow solids and liquids from the start?
2) is it difficult to make the swallowing movement?
3) is swallowing painful? (odynophagia)
4) is the dysphagia intermittent or constant? is it getting worse?
5) does the neck bulge or gurgle on drinking?
TYPES OF DYSPHAGIA
i) what must be queried in dysphagia?
ii) what is the cause of the problem if it is for solids and liquids? what about only solids?
iii) what test should be ordered if there is oesophageal dysphagia?
iv) where are the abnormalities in oropharyngeal dysphagia? (3) name three things that can cause it
v) what is it called if the neck buldges or gugles on drinking?
i) cancer
ii) solids and liquids - neuromuscular
just solids - mechanical obstruc
iii) OGD or barium swallow
iv) oropharyngeal - abnorm in muscles, nerves or structures of oral cav or pharynx (issue with initiation of swallow)
- caused by neuro things - stroke, PD, myasthenia gravis
v) pharyngeal pouch > weakness between muscles makes a pouch
OESOPHAGEAL CANCER
i) is it more common in M or F? what is the most common presenting symptom?
ii) name two criteria that warrant an urgent OGD under 2WW? what imaging can look at distant mets? what can look at penetration into oes wall?
iii) what is the 5year survival? why?
iv) what staging system is used? what is mainstay tx for SCC? how are adenocarcinomas treated?
v) what surgical procedure can be done? which medical tx can be given?name three complications of stenting
vi) name three complications of the operation? what is a major problem post op? what is 5 year survival?
i) more common in males
- dysphagia most common symptom
ii) ysphagia or patient >55yrs with weight loss and upper abdo pain or reflux > upper GI endoscopy (OGD) within 2 weeks
- CT chest abdo pelvis and PET CT to look for distant mets
- endoscopic US to measure penetration into oes wall and biopsy LNs
iii) 5year survival is 10-15%
- presents late
iv) TNM staging
- SCC > upper oes are difficult to operate on and chemo is usually mainstay
- adeno > neoadj chemo or chemo and RT followed by oes resection
v) oesophagectomy - take out oes and connect stomach to it
- can give chemo/RT
- stenting can increase pain, may migrate (bowel obstruc), tumour perforation or bleeding
vi) anastomotic leak, reoperation pneumonia, death
- post op nutrition is a major problem > feed into small bowel (feeding jejunostomy)
- overall 5 year survival is 5-10%
OESOPHAGEAL CANCER
i) what are the two main types?
ii) which part of the oes does each type affect?
iii) name two RFs for each type
iv) which type is most common in the west?
i) Squamous cell carcinoma - affects upper 2/3 oes
- RFs are smoking and alcohol
Adenocarcinoma - affects lower 1/3
- RFs are GORD, barrets oes, obesity
- adenocarcinoma is most common in the west
GORD
i) what happens? is it more common in M or F? name four risk factors? which classification system is used?
ii) what does the lower oes sphincter normally do? what happens in GORD? how is the oes mucosa damaged?
iii) what is the main symptom? when is this the worst? name four other symptoms? name four red flag symptoms - what should be investigated for?
iv) is exam usually remarkable? what % will already have barrets oes?
v) what is the gold standard investigation for diagnosis? what does this comprise of? what score is given? what investigation is done to exclude malignancy - when would this be necessary?
i) gastric acid from stomach leaks up into the oes
- 2:1 M:F
- Los angeles classification - size of breaks in oes (grade A-D)
- RF = age, obese, male, alcohol, smoking, caffiene, spicy food
ii) lower oes sphincter controls passage of contents from oes to stomach - - in GORD more sphincter relax therefore gastric contents reflux into the oes
- refluxed acid results in pain and mucosal damage to the oes
iii) main symptom us chest pain (burning retrosternal sensation) worse after meals, lying down, bending over or straining (relieved by antacids)
- excess belching, odynophagia, chronic or nocturnal cough
- red flag symptoms = dysphagia, weght loss, early satiety, malaise, loss of appetite - investigate for malignancy
iv) examination unremarkable - 10% have barrets oes
v) 24hr pH monitoring is gold standard in dx - when medical tx (PPI) has failied and surgery is being considered
- 24hr pH monitor - assess criteria such as amount of time acid is present in oes anc correlation between acid and symptoms > de meester score to determine correlation bet symptoms and reflux
- upper GI endoscopy to exclude malig and investigate for complications - not required in absence of red flag symptoms