Upper GI surgery

Question 1

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?

Answer 1

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

Question 2

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

Answer 2

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

Question 3

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?

Answer 3

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

Question 4

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?

Answer 4

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)

Question 5

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

Answer 5

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

Question 6

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?

Answer 6

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

Question 7

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?

Answer 7

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)

Question 8

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?

Answer 8

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

Question 9

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

Answer 9

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

Question 10

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?

Answer 10

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

Question 11

DYSPHAGIA

i) what are the five key questions to ask?

Answer 11

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?

Question 12

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?

Answer 12

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

Question 13

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?

Answer 13

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%

Question 14

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?

Answer 14

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

Question 15

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?

Answer 15

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

Question 16

ACHALASIA

i) what is it?
ii) how are peristalsis and lower oes sphincter ffected? is it painful?
iii) name two investigations that can be done
iv) what drug can be given? what can be done endoscopically?
v) what is the appearance of the oes?

Answer 16

i) oes dysmotility syndrome

ii) decreased peristalsis and increased LES tone
- is often painful

iii) can do barium swallow, manometry

iv) give calcium channel blocker
- dilatation by cutting the muscle surgically

v) balloon oes with bird beak at end (thickened muscle at the end)

Question 17

DYSPEPSIA

i) what is it?
ii) name four indications for investigating dyspepsia
iii) what two investigations can be done? what needs to be ruled out?

Answer 17

i) indigestion
ii) new dyspepsia after 40, insidious onset (Anaemia, anorexia, asthenia (lack of energy)), obstruction eg vomiting, bleeding, perforation

iii) OGD then CT chest/abdo
- need to rule out gastric cancer

Question 18

GASTRIC CANCER

i) name two modalities that can be used to stage
ii) what are 75% of gastric cancers? what are 24%
iii) name four risk factors

Answer 18

i) EUS, PET, laparoscopy

ii) 75% are adenocarcinoma
25% are lymphoma

iii) chronic gastritis, h pylori infection, previous gastrctomy, diet (high smoked and salted food, nitrites), smoking

Question 19

CHRONIC PANCREATITIS

i) what is it? how does it affect M compare to F? what is the main cause? name two less common causes?
ii) what is the main symptom? where is pain typically felt? name two things it can also present with?
iii) which areas will be tender on examination? why do some patients get concurrent pseudocysts?

Answer 19

i) chronic fibro-inflammatory disease of the pancreas > progressive and irreversible damage to the parenchyma
- M:F of 4:1 / avg age onset is 40yrs
- main cause is chronic alcohol abuse or idiopathic
- less commonly caused by metabolic, infection, hereditary, AI, congenital

ii) main symptom is chronic pain > recurring attacks of chronic pancreatitis (acute on chronic)
- pain typically in epigastrium and back and often assoc with N+V
- may also px with endocrine insufficiency (IOL damage)/exocrine insufficiency (acinar damage)

iii) tender epigastrium O/E and significant cachexia
- may get concurrent pseudocysts > mass effect eg biliary obstruc or gastric outlet obstruc

Question 20

CHRONIC PANCREATITIS INVESTIGATION AND TX

i) which two blood markers may be tested but not raised? how can endocrine function be checked? what mau LFTs show?
ii) what is faecal elastase? what levels are seen in CP?
iii) name two imaging techniques that may be used
iv) what is the only definitive management? what is the mainstay of tx?
v) what should be given if exocrine dysfunc?

Answer 20

i) serum amylase/lipase - not usually raised
- check blood glucose (check endocrine function) and LFTs (obstructive jaundice)

ii) faecal elastase level (prod by panc and secreted into bowel to aid digestion) > low in most cases
iii) CT. USS, MRI (MRCP (images bil tree and panc ducts)

iv) only definitive management is to treat any reversible underlying cause eg alcohol cessation or statins for hyperlipid
- analgesia is usually the mainstay of treatment (use neuropathic analgesia eg pregabalin)

v) if exocrine dysfunc > malabsorption > enxume replacement and vitamin supplements

Question 21

PANCREATIC CANCER

i) what age are 80% of cases found in? what type are most - which functional part of pancreas are they found?
ii) which anatomical area are 60% found? name three risk factors? name a specific risk factor that is strongly associated with panc cancer?
iii) what do 90% of patient present with due to compression of bile duct? name two other presenting features
iv) how may patient appear on exam? what may be felt in abdo - whaich region?
v) what is courvoisers law? which pathology does this aim to rule out?

Answer 21

i) 80% of cases are 60-80yrs
- most are ductal carcinoma from exocrine portion of panc

ii) 60% arise in head of panc (those at the tail are more likely to dx late)
- RFs - smoking, chronic pancreatitis, dietary factors eg high red meat, low veg
- late onset diabetes mellitus is a RF (dx with diabetes >50yrs have 8x risk of dev)

iii) specific clinical features depend on the site of the tumour
- obstructive jaundice (due to compression of common bile duct) - pres in 90% of cases (painless)
- weight loss due to metabolic effects/2nd to exocrine dysfunction
- non spec abdo pain - due to invasion of coeliac plexus or 2nd to pancreatitis

iv) patient may appear cachetic, malnourished, jaundiced
- may palpate an abdo mass in epigastric region and an enlarged GB

v) courvoiser law - pres of jaundice and enlarged GB - strong suspic of biliary tree or panc malignancy (unlikely to be gallstones)

Question 22

PANCREATIC CANCER TREATMENT

i) what may be seen on FBC/LFT? which tumour marker is highly sensitive and specific for pancreatic cancer?
ii) what is gold standard imaging? name three imaging that can be done if unclear dx and what may be seen? what is used for staging/tissue biopsy?
iii) what is the only curative option? what is the name of the procedure that resects the head of the pancreas?
iv) what should all surgical patient recieve before operation?
v) what is mainstay of treatment for met disease

Answer 22

i) FBC - anaemia/thrombocytopenia
- LFT - raised bilirubin, ALP and GGT
- CA19-9 sens and spec but better for tx response rather than dx

ii) can do US, CT, PET CT or MRCP if unclear dx
abdo US - panc mass or dilated billiary tree/hepatic mets or ascites
- CT is gold standard for prelim dx
- endoscopic US for staging/biopsy

iii) radical resection is the only curative option
(classified as resectable, borderline resectable or locally advanced dep on contact between tumour and surrounding vessels)
- Surgery to head of panc = whipples (pancduodenectomy)
- body/tail - distal pancreatectomy

iv) all surgical pts should recieve adjuvant chemo with gemcitabine or 5-FU
v) if met disease > palliative chemo is mainstay

Question 23

GASTRIC CANCER

i) where do 90% arise from? what histol subtype are they?
ii) name four symptoms? is much usually found on examination? what is troisers sign? what may be felt in late disease?
iii) what is the primary investigation for gastric cancer? name two indications for the investigation? name three tests that may done on biopsy samples? is PET routinely used?
iv) what is mainstay treatment? what is done in proximal tumours? what is done for distal tumours? what type of recontruction is then done? what may early stage T1a tumours be offered?
v) name three complications? what is 10 year survival rate?

Answer 23

i) 90% arise from the gastric mucosa and are adenocarcinomas

ii) Vague and non specific symptoms - dyspepsia (indigestion)
* dysphagia
* early satiety, vomiting, melanea
* anorexia, WL, anaemia > late stage disease
* absence of clinical signs on exam
- troisier sign = palpable left supraclavic node > met abdo malignancy
- met > hepatomegaly, ascites, jaundice, acanthosis nigracans (dark skin crease)
- epigastric mass may be felt in late stage disease

iii) primary investigation is upper GI endoscopy (OGD) for vis and biopsy
- urgent OGD if new onset dysphagia or aged >55yrs with weight loss, upper abdo pain, reflux or dyspepsia
- send biopsies for histol,, CLO test (hpylori), HER2/neu expression for targeted therapies
- PET not really used as gastric cancers dont take up radioactive tracer well

iv) curative tx mainstay is surgery > neoadj chemo then surgery then adj chemo
- proximinal gastric cancer > total gastrectomy
- distal gastric cancer (antrum or pylorus) > subtotal gastrectomy
- reconstruct with roux en Y reconstruc (small bowel connected to oes)
- T1a tumours may bbe offered endoscopic mucosal resection

v) gastric outlet obstruction, iron defic anaemia, perforation, malnutrition
10 year survival is 15% but stage dependent

Question 24

HIATUS HERNIA

i) what is a hernia? what is a hiatus hernia? what most commonly herniates?
ii) what are the two main stypes? what happens in each? which one is a true hernia?
iii) what is the biggest RF? name three others
iv) do most patients present with symptoms? name the most common symptom? name four other symptoms? what may be heard in the chest? is clinical exam usually remarkable?
v) what is gold standard investigation? what does it show? name another investigation that may be done

Answer 24

i) hernia = protrusion of whole or part of an organ through the wall/cavity that contains it into an abnormal position
- hiatus hernia = protrusion of organ from abdo cavity into thorax through the oes hiatus
- typically stomach herniating (can be small bowel, colon, mesentery)

II) classified into

• sliding hiatus hernia (80%) > gastro oes junction, abdo oesophagus and cardia of stomach move/slide up through the diaphragmatic hiatus into the thorax
• rolling/para oes hernia (20%) - upward movement of gastric fundus > lies alongside a normal positioned gastro oes junction > bubble of stomach insude thorax = true hernia with peritoneal sac

iii) age is the biggest RF, pregnancy, obesity and ascites due to increased intra abdo pressure and superior displac of the viscera

iv) most are asymp
- most common symp > gastro oes reflux symptoms such as burning epigastric pain, worse when laying flat
- vomiting, weight loss, bleeding/anaemia, hiccups or palpitations as it can irritate disphraghm or percardial sac, swallowing difficulties
- clinical exam is usually normal
- if large then bowel sounds may be auscultated in the chest

Question 25

HIATUS HERNIA TREATMENT

i) what is first line pharma treatment? what does this do? when should it be taken? name three lifestyle advice that may be given? which two things can inhibit lower oes sphincter function therefore worsen symptoms?
ii) name three indications for surgical management?
iii) what happens in a cruroplasty? what happens in fundoplication?
iv) name three complications? what are rolling HH prone to?
v) name a complication that results in a surgical emergency? what is borchardts triad?

Answer 25

i) first line pharma management is PPI eg omeprazole to reduced acid secretion and control symptoms > take in morning before food
- lifestyle advice eg weight loss, alteration of diet, sleep with head of bed raised
- smoking cessation and reduce alcohol because both inhibit lower oes sphincter func and worsen symptoms

ii) surgical management when remaining symptomatic after medical therapy, increased risk of strangulation/vlvulus or nutrirtional failure due to gastric outlet obstruc

iii) cruroplasty > hernia is reduced from thorax into the abdomen and hiatus reapprox to right size > mesh to strengthen repair
- fundoplication > gastric fundus is wrapped around lower oes and stitched in place > strengthen LOS to prevent reflux and keep GOJ in place below the diaphragm

iv) recurrence of hernia, bloating due to inability to belch, dysphagia if fundoplication is too tight or crural repair too narrow, fundal necrosis - blood supp via left gastric is disrupted > sx emergency
- rolling hiatus hernia are prone to incarceration and strangulation

v) gastric volvulus (stomach twists on itself 180 > obstruc of gastric passage and tissue necrosis) sx emergency
- volvulus can present with borchardts triad > severe epigastric pain, retching but not vomit, inability to pass an NG tube

Question 26

GORD TREATMENT

i) what are the first steps in management? what are first line pharma tx? does this work for most patients?
ii) when do symptoms recur? what is done to prevent this?
iii) when is a patient surgically managed? (3) name three things surgical management is good for
iv) what surgical procedure is done? what is the result of this? what are the main SE of the surgery? (3) how long does it usually take for these to settle?
v) name four complications? what is 7yr risk of adenocarcinoma?

Answer 26

i) start with conservative steps > avoid ppts, weight loss and smoking cessation
- PPI are first line and are effective for most patients

ii) symptoms tend to recur after stopping PPIs so most patients stay on them lifelong

iii) sx management if fail to respond to medical, patient preference, patients with complications eg recurrent pneumonia
- sx more effective than medical tx for symp relief, QOL and cost

iv) funodplication > GOJ and hiatus are dissected and the fundus is wrapped around the GOJ to create a new lower oes sphincter
- main SEs are dysphagia, bloating, inability to vomit = usually settle after 6 weeks

v) aspiration pneumonia, barrets oes, oes stricture, oes cancer
- 7yr risk of adenocarcinoma is 0.1% where initial endoscopy is absent of strictures, barrets metaplasia

Question 27

CHOLECYSTITIS

i) what is it? what is it usually caused by? what are the 5 RFs? what three types of stone may be found
ii) name two areas pain will be felt? what may this be associated with? which sign will be positive? what is guarding a sign of?
iii) which imaging is the most sensitive? what is gold standard? what may be seen in FBC/CRP? what may LFT show? will ALT/bilirubin be affected?
iv) what three drugs should be started after diagnosis? what can be given to relax smooth muscle of the biliary tree? how quickly should lap chole be done? what can be done if patient isnt fit for sx or isnt responding to abx?

Answer 27

i) nflammation of the gall bladder usually caused by gallstones blocking the cystic duct
- bile is stored in the GB > duodenum when stimulated - gallstones form due to supersaturation of bile
- RFs are 5Fs - fat, female, fertile, forty, family history (+ COCP, preg, haemolytic anaemia)
- three types of stone - cholesterol (excess choles prod), pigment (excess bile pigment prod assoc w haemolytic anaemia), mixed (cholesterol + bile pig)

ii) constant pain in RUQ or epigastrium assoc with signs of inflammation such as fever/lethargy
*tender RUQ O/E with positive murphys sign (palpate under R costal margin, ask pt to breathe in (GB contacts hand) and pt feels pain. Repeat on LHS and should not feel pain = +ve)
- guarding may indicate GB perforation

iii) trans-abdo US most sensitive for gallstones and used first line
- gold standard for GS is MRCP
- raised WCC and CRP
- LFT may show raised ALP (cholestasis) but normal ALT and bili

iv) start on IV abx (co amox/metronidazole), Prescribe concurrent analgesia and anti emetics
- may give buscopan to relax sm muscle of bil tree > may pass the stone
- laparoscopic cholecystectomy within 1 wk of presenting (NICE) but ideally within 72hrs
- Not fit for sx/responding to abx - percutaneous cholecysostomy to drain infection but GS remain in situ

Question 28

OESOPHAGEAL STRICTURE

i) what is it? how can you differentiate between malignant/benign? how does a simple stricture appear? how does a complex stricture appear?
ii) name three risk factors? name four causes
iii) name three symptoms? name three investigations that can be done?
iv) what pharma treatment is give? what is done if this is unsucessful? what can be done for a complex stricture?

Answer 28

i) abnormal tightening or narrowing of oes
- malig get worse quickly and benign progress slowly
- simple - smaller, with smooth surfaces and leave a wider opening in the oes
- complex > longer and leave narrower opening, not striahgt/symm and leave uneven surfaces

ii) RF - ETOH use, GORD, hiatus hernia, PUD and hx of dysphagia
- caused by eosinophilic eoesphagitis (immune reac > inflam in oes), oes cancer, GORD, RT to head or neck, surgery, some abx or NSAIDs

iii) burning sensation in neck or throat, dysphagia, feeling of food getting stuck in throat, frequent episodes of choking
- investigations = barium swallow > xray
- US - How thick oes wall has become > how much narrowing is present
- endoscopy - can also biopsy
- oes manometry - examines muscles and sphincter

iv) antacids
- if antacids unsuccesful - oes dilation via endoscopy - use balloon or dilator to widen the narrow area
- complex stricture > metal oes stent (strong but can cause pain and need to be changed every few months)
- biodegrad stent > not as strong as metal stents but more comfortable

Question 29

REFLUX OESOPHAGITIS

i) what is it? what is the most common cause?
ii) how can obesity cause it? name four risk factors? what classification is used?
iii) what type of chest pain is felt? name three other symptoms?
iv) what investigation is done? which less sensitive investigation may also be done?
v) name three lifestyle changes that may be reccomended? which pharma drug is given? what is done if unresponsive to medical therapy?
vi) name four complications

Answer 29

• inflammation of oesophagus and macroscopic damage to lining of oes > breaks in lining or ulceration
• GORD is the most common cause

ii) Obesity, increased intra ab pressure eg preg or ascities
- RFs - male, over 50, FH, central obesity, smoking, delayed gastric emptying, hiatus hernia, NAFLD
- los angeles classification

iii) chest pain (retrosternal), acid regurgitation, heartburn, odynophagia (painful swallow), dysphagia, may cause bleeding

iv) OGD - vis inflammation and severity can be determined - can take biopsy and can treat bleeding
- barium swallow (less sensitive than OGD)

v) lifestyle change - smoking cessation, avoid chocolate, caffeiene, spicy food, elevate head at night
- pharma tx > PPIs
- if non responsive to medical therapy > surgery (funodplication)

vi) barrets oesophagus > endoscopy 8-10 weeks post PPI to check for healing
- lower oes rings (schatzi rings) > dilate to treat
- peptic structure in older patients
- oes adenocarcinoma

Question 30

UPPER GI BLEEDING

i) name three oes causes? name four gastric causes? what two risk assess scores are used?
ii) what is haematemesis? what does frank blood indicate? what does coffee ground indicate? how else may a patient present? (2)
iii) name three ways to assess for signs of hypovol shock? what is the most common source of bleeding? how quick should an UGI endoscopy be done?

Answer 30

i) oes causes - varices (2nd to portal HTN) oesophagitis, mallory-weiss tear, oes cancer
- gastric causes - peptic/duo ulcer (HP/NSAIDs), gastritis (NSAIDs, alcohol), angiodysplasia, gastric cancer
- risk asess with blatchford score (first assess) and rockall score (after endoscopy)

ii) Haematemesis - bloody vomit orig from site proximal to distal duo
- frank haem (pre stomach), coffee ground haem (post stomach)
- may present with symptoms of shock or melanea

iii) hypovol shock - tachy, hypotensive, low urine output and cool peripheries
- identify cause of bleeds - most common are ulcers and variceal
- urgent UGI endoscopy 24hrs post presentation

i

Question 31

UPPER GI BLEEDING MANAGEMENT

i) name two things to be given if patient is in shock? when should plats be transfused? what APTT/PT warrants FFP?
ii) name three things that can be done via UGI endoscopy to treat the bleed? name three drugs that can be given if variceal bleed is suspected?
iii) what drug should be given if patient is high risk? name two other methods that may be used to stop the bleeding

Answer 31

i) O2, IV fluid challenge if in shock
- blood products if actively bleeding
- plat transfuse if plats <50
- if APTT/PT >1,5 then give FFP

ii) UGIE - haemmorhage source control, therapy coag, thrombin injection with adrenaline, banding for varicies
- octreotide/terlipressin and prophylax abx for suspected variceal bleed

iii) HR patient - start 72 hr IV PPI infusion
- consider other methods to stop bleeding eg balloon tamponade or transjuglar intrahepatic porto systemic shunting

Question 32

MELAENA

i) what is it? how does it appear? what is the most common cause? name three other causes
ii) what may it be associated with? (3)name two examinations that can be used to confirm it?
iii) why may FBC be normal initially? which ratio is usually indicative of a UGI bleed? what should be done for all patients?
iv) what is the definitive investigation? what imaging technique can be used to assess active bleeding?
v) what should be the first thing done in treatment? what should be arranged when the patient is stable? what is done for PUD cause and oes varices cause?
vi) what can be inserted if there are uncontrolled oes varices? what can be done in upper GI malig? when should blood be transfused?

Answer 32

i) black tarry stools > result of upper GI bleeding
- dark and smelly - alteration and degradation of blood by intestinal enzymes
- PUD is most common cause - suspect in those with known active PUD, NSAID/steroid use, dyspepsia symptoms, HP positive
also caused by
- oes varices > dilat of portosystemic anastomoses in oes (mostly caused by alcoholic liver disease)
- upper GI malignancy
- mallory weiss tear, meckles diverticulum, vascular malforms

ii) jet black, tar like, sticky stools that may be assoc with haematemesis, abdo pain, dyspep, dysphagia or odynophagia
- DRE and abdo exam for epigastric tendernes sor perotonism, hepatomegaly or stigmata of liver disease
- drop in Hb or rise un urea:cr ratio - indicative of UGI bleed
- Group and save for all patients (espec variceal)

iv) OGD is definitive investigation
- CT abdo ith IV contrast (trople phase) to assess active bleeding

v) A-E approach first
- once stable > arrange endoscopy
- if PUD - inject adrenaline and cauterise the bleed > give high IV dose PPI to control acidic enviro
- if oes varices - need quick mx (same time as A-E) - endoscopic banding is definitive but can be difficult, prophylactic abx w somatostatin analog (terlipressin/ocreotide) to reduce splanchnic blood flow > reduce bleeding

vi) sengstaken blakemore tube for uncontrolled cases of oes varices > insert at level of varices and inflate to compress the bleed temporarily
- upper GI malig > biopsy and long term sx and onc management
- blood transfusion if haem unstable