Title: Gastroenterology and Surgery

Q: Three types of functional cysts
A: Graafian follicles - Ruptures at ovulation "Mittelschmerz"
Corpus luteum cysts
Haemorrhagic cyst

Q: Non-benign ovarian cysts
A: Dermoid cysts
Endometriomas (chocolate cysts)
Cystadenomas

Q: Risk factors for adnexal torsion
A: Pregnancy
Large ovarian cysts/tumors
Chemical induction of ovulation
Recent intense exercise

Q: What proportion of fibroids are symptomatic?
A: 50%

Q: What proportion of patients with mesenteric ischaemia have normal lactate on presentation?
A: 25%

Q: How sensitive and specific is serum lipase for pancreatitis?
A: 90% and 93%

Q: What is the sensitivity of plain AXR for SBO?
A: 50%

Q: What is the sensitivity of upright CXR for free air?
A: 30%

Q: What is the specificity of non-contrast CT for appendicitis?
A: 97%

Q: Is non-contrast CT more useful in the diagnosis of appendicitis in fat or skinny people?
A: Fat people as it provides contrast

Q: When is PO contrast helpful in abdominal CT?
A: For GI perforation, abscess or fistula. NOT for ischaemia as limits contrast enhancement of bowel wall

Q: What proportion of the elderly have a typical presentation of appendicitis?
A: <20%

Q: What proportion of mesenteric ischaemia suffer diarrhoea?
A: 40%

Q: Most common surgical diagnoses in the elderly with abdo pain?
A: Cholecystitis
SBO
Perforated viscous
Appendicitis
LBO

Q: Complications of Roux-En-Y
A: Anastomotic leak
Bowel obstruction (volvulus of Roux limb or internal hernia)
Cholelithiasis
Dumping syndrome
Metabolic complications (B12, iron, thiamine)
Stenosis of gastrojejunostomy site

Q: How does bowel obstruction present after Roux-En-Y?
A: Bilious emesis if common channel obstruction
Severe pain and peritonism if gastroduodenal limb dilates/perforates

Q: What is dumping syndrome?
A: Rapid post-prandial gastric emptying with release of gastric hormones and splanchnic vasodilation
Early symptoms (30-60min) - Nausea, vomiting, bloating, sweating, diarrhoea
Late (1-3hrs): Hyperinsulinaemia and hypoglycaemia

Q: Management of epiploic appendigitis
A: Supportive care
ANalgesia
No antibiotics

Q: What is tertiary peritonitis?
A: Peritonitis that persists 48 hours after apparent source control
Usually S. epidermidis, enterobacter, Enterococci, Pseudomonas or Candida

Q: What is intra-abdominal compartment syndrome?
A: Intra-abdominal hypertension >12mmHg
IA compartment syndrome >20mmHg

Q: Mortality of abdominal compartment syndrome?
A: 50%

Q: What is Ogilvie syndrome?
A: Caecal dilatation from large bowel pseudo-obstruction

Q: Treatment of Ogilvie syndrome
A: Colonoscopic decompression
Neostigmine
Avoid opioids/anticholinergics/electrolyte disturbance

Q: What proportion of mesenteric ischaemia suffer nausea/vomiting?
A: 75%

Q: Causes of mesenteric ischaemia
A: Embolic (50%)
Thrombotic (20%)
Non-occlusive (20%)
Venous thrombosis (10%)

Q: How does sigmoid volvulus present on XR?
A: Bent inner tube
Bird beak taper at transition point on rectal contrast enema

Q: Treatment of sigmoid volvulus
A: Sigmoidoscopic decompression and rectal tube
Corrective repair at some stage if fit for surgery

Q: Mortality rate of sigmoid volvulus
A: 20% (50% if gangrenous)

Q: How does caecal volvulus present on XR
A: Coffee bean in younger patients

Q: complications of haemorrhoids
A: Inflammation
Itch
Thrombosis
Bleeding
Prolapse
Ulceration
Ischaemia

Q: What are internal haemorrhoids?
A: Originate proximal to dentate line
Always at 2-, 5- and 9- o'clock when viewed prone
Not readily palpable or visible unless prolapsed
Covered in columnar epithelium of surrounding anal canal
Viscerally innervated

Q: What are external haemorrhoids?
A: Distal to dentate line and can be any location on clock
Visible on external inspection
Covered in stratified squamous skin of peri-anal region
Exquisite sensory somatic innervation

Q: Do haemorrhoids cause iron deficiency anaemia?
A: Very rarely. Rule out colonic malignancy (esp. if >40yo)

Q: When do haemorrhoids cause pain?
A: Thrombosed or strangulated fourth-degree internal haemorrhoids

Q: How do uncomplicated internal haemorrhoids present?
A: Painless, bright red bleeding with defecation

Q: Grades of internal haemorrhoids?
A: Grade 1 - Painless bleeding. Swelling above dentate line
Grade 2 - Prolapse with spontaneous reduction
Grade 3 - Prolapse with manual reduction
Grade 4 - Irreducible

Q: Treatment of haemorrhoids
A: Simple analgesia
Topical analgesics/steroids
Stool softeners
Bulk laxatives
Sitz baths 15min TDS
Surgical outpatient referral for symptomatic ones
Manually reduce prolapsed ones if possible
Topical lignocaine OR ISMN ointment for acutely thrombosed ones
No real indication for acute incision of thrombosed

Q: How long do thrombosed external haemorrhoids take to resolve?
A: 1 week with conservative management

Q: CI to ED thrombosed external haemorrhoid excision?
A: Pregnancy
Liver disease
Immunosuppression
Possible internal haemorrhoids
Children
Anticoagulated
Coagulopathy

Q: Significance of non-midline anal fissures?
A: More likely IBD, SCC, adenocarcinoma, syphilitic, Chlamydia, Gonorrhoea, HIV, tuberculous ulcer

Q: Typical anal fissures in Crohn's
A: Multiple, non-midline, painless

Q: Causes of fistula-in-ano?
A: Anorectal abscess
IBD
Colonic malignancy
Radiation
Leukaemia
STI

Q: What is Goodsall's rule?
A: Anterior opening fistulas tend to follow a straight path to anal canal
Posterior opening fistulas tend to follow curved path to anal canal

Q: Treatment of fistula in ano
A: Analgesics
IV fluids
Cipro + Metronidazole
Surgical referral +- CT pelvis/MRI pelvis/Trans-anal USS

Q: Presentation of anorectal abscess
A: Dull throbbing constant pain
Usually younger males
Pain worse before defecation and relieved afterwards but persists between openings (unlike anal fissures)

Q: Which patients with anorectal abscess need antibiotics?
A: Elderly, immunosuppressed, febrile, septic, valvular heart disease, cellulitis

Q: Causes of proctitis
A: Radiation
Autoimmune conditions
Vasculitis
Ischaemia
Gonorrhoea
Chlamydia
Syphilis
HSV 2
HIV
HPV

Q: Primary syphilitic proctitis presentation
A: Chancres at anal verge +- inguinal adenopathy

Q: Secondary syphilitic proctitis
A: Condylomata lata at perianal region

Q: What causes anorectal herpes?
A: HSV-2

Q: Describe acute radiation proctitis
A: Tenesmus, diarrhoea, itch, bleeding within 6 months of radiotherapy to pelvis

Q: Anal canal vs. anal margin carcinomas?
A: Anal canal far worse, metastasise early to perirectal, mesenteric and paravertebral nodes

Q: Recurrence rate of pilonidal sinus?
A: 20-40%

Q: Lifetime risk of appendicitis in males and females?
A: 12% and 25%

Q: Is appendicitis more common in pregnancy?
A: No

Q: Rate of appendicitis in pregnancy?
A: 1/1500

Q: How does retrocaecal appendicitis present?
A: RUQ or pelvic pain

Q: What is the most common site of appendicitis pain in pregnancy?
A: RIF still

Q: What is psoas sign?
A: Pain in abdomen with extension of right leg in left lateral position

Q: Sensitivity modified Alvarado (Mantrels)
A: 72% (vs 93% for clinical judgement)

Q: Alvarado score components
A: Migratory RLQ pain
Anorexia
Nausea/vomiting
RLQ tenderness (2)
Rebound tenderness in RLQ
Fever  > 37.5
WCC >10 (2)

Q: Specificity of high risk Alvarado score?
A: 81%

Q: Sensitivity of WCC and CRP for appendicitis?
A: Up to 98%

Q: Normal maximal diameter of appendix on USS
A: 6mm

Q: Sensitivity of CT for appendicitis
A: 95%

Q: Sensitivity of USS for appendicitis
A: 86%

Q: Which patients are most at risk of appendicitis perforation?
A: Elderly, pregnant, children <5

Q: How much more common is appendiceal rupture in pregnancy?
A: 3x (2nd/3rd mostly as gravid uterus stretches omentum/less sensitive)

Q: Is USS more specific or sensitive for appendicitis?
A: Specific

Q: Is USS useful in pregnancy for appendicitis?
A: Equally as sensitive and specific

Q: Pregnancy-specific complications of appendicitis?
A: Miscarriage, premature labor, fetal death

Q: Causes of duodenal obstruction
A: Duodenal ulcer
Stenosis
Foreign body
Stricture
Superior mesenteric artery syndrome

Q: Causes of small bowel obstruction
A: Adhesions
Hernias
Intussusception
Lymphoma
Stricture

Q: Causes of large bowel obstruction
A: Malignancy
Diverticulosis
Faecal impaction
Ulcerative colitis
Volvulus
Intussusception
Pseudoobstruction

Q: Bowel sounds in ileus?
A: Decreased

Q: Bowel sounds in obstruction
A: High-pitched

Q: What does WCC >20 suggest in bowel obstruction?
A: Peritonism, perforation, gangrenous bowel, intra-abdominal abscess

Q: What does WCC >40 suggest in bowel obstruction?
A: Mesenteric vascular occlusion

Q: Define toxic megacolon?
A: Diameter >6cm in IBD or C. diff

Q: Sensitivity of AXR for bowel obstruction?
A: 50%

Q: What number of air-fluid levels is pathological?
A: >5

Q: What is Rigler's sign?
A: Double wall sign seen on AXR with intra-peritoneal free air
Air on both sides of intestinal wall

Q: What proportion of kidney stones are radio-opaque?
A: 80%

Q: What proportion of gallstones are radio-opaque?
A: 20%

Q: Rome criteria for constipation
A: 2 or more of:
Straining >25% of the time
Hard stools >25% of the time
Incomplete evacuation >25% of the time
<3 bowel motions per week

Q: Red flags of acute constipation
A: Sudden onset
Nausea/vomiting
Severe abdominal pain
Distension
Unexplained weight loss
PR bleeding
Unexplained iron deficiency
FHx of colon cancer
Fever
Change in stool calibre

Q: 4 mechanisms of diarrhoea
A: Increased osmotic load
Enhanced intestinal motility
Secretory diarrhoea
Reduced absorption

Q: How is fluid absorbed by the bowel?
A: Passive via sodium
Active via glucose

Q: How does osmotic diarrhoea present?
A: Resolves with fasting

Q: How does secretory diarrhoea present?
A: Does not resolve with fasting

Q: Diagnostic yield of stool culture?
A: <5%

Q: When is stool MCS recommended in diarrhoea?
A: Unwell child
Toxic, dehydrated, febrile patients
Diarrhoeal illness >3 days
Blood or pus in stools
Immunocompromised

Q: When is stool OCP advised?
A: Travellers exposed to untreated water
Diarrhoea >7 days

Q: False negative rate of C. diff toxin testing?
A: 10%

Q: How common is traveller's diarrhoea?
A: 40% of travellers to developing countries within 2 weeks

Q: What is the probability of bacterial diarrhoea if returned traveller?
A: 80%

Q: Treatment of traveller's diarrhoea?
A: Cipro 500mg BD for 3/7
 - Not for E. coli 0157:H7 due to increased risk of HUS

Q: Benefit of cipro for traveller's diarrhoea?
A: Reduces duration by around 1 day

Q: Treatment of C. diff
A: Mild - Stop antibiotic + Metronidazole 400mg TDS for 14 days or 500mg IV BD if NBM
Moderate (WCC >15) - Vancomycin 125mg PO QID for 14 days
Severe disease - IV Metronidazole + PO vancomycin
Emergency colectomy if complications

Q: Treatment of Entamoeba histolytica
A: Metronidazole 750mg PO TDS for 10 days

Q: Treatment of Giardia
A: Tinidazole 2g PO stat

Q: What proportion of antibiotic-associated diarrhoea is due to C.diff?
A: 10-20%

Q: Risk factors for C. diff
A: Recent hospitalisation, broad-spectrum antibiotic use (PO or IV), chemo, Gi surgery, critical illness, increased age

Q: What proportion of hospitalised patients are C. diff colonised?
A: 10-25%

Q: Which antibiotics cause most risk of C. diff?
A: Clindamycin
Cephalosporins
Ampicillin
Fluoroquinolones

Q: When does C. diff cause symptoms?
A: Usually 7-10 days from initiation of antibiotics (but up to 60 days)

Q: How does C. diff present?
A: Frequent, mucoid, watery stools +- abdominal pain and leukocytosis
Can present with paralytic ileus

Q: Risk of toxic megacolon or colonic perforation with C. diff?
A: 1-3%

Q: Stool culture for C. diff sensitivity and specificity
A: Sensitivity approaches 100% but not specific as may be present but not causing disease

Q: Sensitivity and specificity of C. diff toxin testing?
A: Both 75-100%

Q: Do alcohol rubs eliminate C. diff?
A: Not the spores

Q: Which IBD has more extraintestinal manifestations and systemic features?
A: Crohn's

Q: Does CD or UC have higher risk of colonic carcinoma?
A: Equal

Q: What proportion of Crohn's is isolated to the colon?
A: 20%

Q: What proportion of Crohn's have extraintestinal manifestations?
A: 40%

Q: Initial therapy of Crohns exacerbation
A: Rehydration
Analgesia
NG
PipTaz/triples
IV steroids (Hydrocortisone 300mg daily for severe)

Q: Biologics use in Crohns
A: Anti-TNFalpha (infliximab, adalimumab) for resistent moderate-severe disease

Q: Risks of anti-TNFalpha biologics?
A: Lymphoma, TB, infection, progressive multifocal leukoencephalopathy

Q: Complications of Crohns
A: Abscess formation
Fistulae
Obstruction
Perianal above
Major GI bleeding
Toxic megacolon
Vitamin deficiency
Electrolyte deficiency
Complications of immunosuppressive therapy
Bowel cancer

Q: Presentation of UC
A: ABdominal pain
Bloody diarrhoea
Tenesmus

Q: Define mild UC
A: <4 motions per day, no systemic symptoms, few extraintestinal manifestations

Q: Define moderate UC
A: Good response to therapy, usually extends to splenic flexure

Q: Define severe UC
A: Frequent bowel motions
Anaemia
Weight loss
Systemic features
Extraintestinal manifestations

Q: Extra-intestinal manifestations of UC
A: Arthritis - AS, sacroiliitis
Uveitis
Erythema nodosum
Pyoderma gangrenosum
Cholelithiasis
Primary sclerosing cholangitis
Cholangiocarcinoma
DVT
Portal venous thrombosis
Mesenteric vein thrombosis
Malnutrition
Chronic anaemia
Nephrolithiasis

Q: DDx of IBD
A: Infectious colitis
Ischaemic colitis
Radiation colitis
Pseudomembranous colitis

Q: DDx of rectal IBD
A: Rectal syphilis
Gonorrhoea
HSV
Entamoeba histolytica
Shigella
Campylobacter

Q: Truelove and Witts criteria
A: Bowel motions per day
Blood in stools
Fever
HR >90
Anaemia
ESR <30 or >30

Q: Increased risk of colonic carcinoma in IBD
A: 10-30x

Q: Testing in HIV or primary immunodeficiency diarrhoea
A: Stool PCR parasite - Giardia, Cryptosporidium, Cyclospora, Isospora, Dientamoeba, Entamoeba, Microsporidia, Histoplasmosis, Cryptococcus
Stool PCR virus - Novovirus, astrovirus, adenovirus, rotavirus, HSV, CMV
Stool PCR bacteria - Salmonella, Shigella, Shiga toxin EHEC, Campylobacter
Stool MCS
C. diff

Q: What proportion of diverticulitis presents with diarrhoea vs. constipation
A: Diarrhoea - 30%
Constipation - 50%

Q: Which patients with suspected diverticulitis need CT?
A: First presentation
Suspicion of complications
Failed conservative management

Q: Follow-up of diverticulitis?
A: All patients need colonoscopy after 6 weeks to rule out carcinoma

Q: Treatment of diverticulitis
A: Uncomplicated (75%) - Augmentin 875/125 BD for 5 days
Complicated (25%) - CT, NBM, fluids, analgesia, IV triples, surgical consult

Q: Success rate of oral augmentin for uncomplicated diverticulitis?
A: 90%

Q: Complications of diverticulitis
A: Stricture
Obstruction
Bleeding
Abscess
Perforation

Q: Differences in younger patients with diverticulitis
A: Thought to be more severe illness
Higher rates of recurrence and complications
Consider surgical referral in all

Q: Meckel's rule of 2's
A: 2% of population
2ft from ileocaecal junction
Symptomatic in 2% of patients

Q: Is diverticula bleeding associated with diverticulitis?
A: No

Q: How long do new trans-abdominal feeding tracts take to mature?
A: 2-3 weeks

Q: Drugs associated with hepatitis
A: Paracetamol
Alcohol
Mushrooms
Vitamin A
Isoniazid
Propylthiouracil
Flucloxacillin
Phenytoin
Valproate
Statins

Q: What suggests fulminant liver failure
A: Encephalopathy, coagulopathy, abnormal fluid shifts, hypoglycaemia, hepatorenal syndrome

Q: O'Grady classification of acute liver failure
A: Hyperacute: Encephalopathy within 7 days of jaundice
ACute: Encephalopathy within 8-28 days of jaundice
Subacute: Encephalopathy 4-26 weeks after jaundice

Q: Causes of hyperacute liver failure
A: Paracetamol, ischaemic, viral, toxins

Q: Prognosis of hyperacute liver failure
A: Greatest degree of coagulopathy, encephalopathy, cerebral oedema, MODS
Greatest chance of spontaneous recovery though

Q: Causes of subacute liver failure
A: Idiopathic, HepB, paracetamol or drug-related usually

Q: Prognosis of subacute liver failure
A: Very poor prognosis despite overall risk of cerebral oedema being less

Q: Incubation period of HepA
A: 15-50 days

Q: Does hepA cause chronic hepatitis?
A: No

Q: What proportion of HepA infections cause acute liver failure?
A: 0.35% (but constitutes 10% of cases)

Q: Diagnosis of acute hepatitis A?
A: anti-HAV IgM

Q: Incubation period of hepatitis B?
A: 1-3 months

Q: Does Hepatitis B cause acute hepatitis?
A: Yes. Just like Hepatitis A

Q: What proportion of adults suffer chronic hepatitis from HepB?
A: 6-10%

Q: What proportion of infants will suffer chronic hepatitis B after acute infection?
A: 90%

Q: How is acute Hepatitis B hepatitis diagnosed?
A: Anti-HBV IgM

Q: Does hepatitis C cause acute hepatitis?
A: 16% symptomatic=

Q: What proportion of hepatitis C infections suffer chronic hepatitis?
A: >75%

Q: Which patients suffer disease from hepatitis D?
A: Superinfection with Hepatitis B (mostly IVDU)

Q: Does Hepatitis E cause acute hepatitis?
A: yes. Does not cause chronic Hepatitis

Q: What proportion of acute liver failure is due to drugs?
A: 25%

Q: What is seronegative acute hepatitis?
A: Once drugs and viruses ruled out

Q: Causes of seronegative acute hepatitis?
A: Acute autoimmune hepatitis (usually lacking the autoantibodies)
Fulminant Wilson's disease
HELLP
Heat shock injury
Ischaemic
Budd-Chiari syndrome

Q: What is Budd-Chiari syndrome?
A: Hepatic vein obstruction

Q: Most common causes of acute on chronic hepatic failure?
A: GI bleed
Spontaneous bacterial peritonitis
Sepsis
Intoxication
Dehydration
Hepatocellular carcinoma
Portal vein thrombosis

Q: Is cerebral oedema more common in acute liver failure or acute on chronic liver failure?
A: Acute liver failure

Q: What ascitic tap findings suggest spontaneous bacterial peritonitis?
A: >250 polymorphs/mm3

Q: Survival rate at 1 month after SBP?
A: 70%

Q: Survival rate at 6 months after first episode SBP?
A: 30%

Q: What proportion of ascitic patients will suffer SBP per year?
A: 30%

Q: What is hepatorenal syndrome?
A: Acute renal failure with normal renal parenchyma in presence of hepatic failure

Q: Modified Parsons-Smith scale of hepatic encephalopathy
A: Stage I - General apathy - GCS 15
Stage 2 - Lethargy, drowsiness, variable orientation, asterixis - GCS 11-15
Stage 3 - Stupor with hyperreflexia, extensor plantars - GCS 8-11
Stage 4 - Coma - GCS <8

Q: DDx of hepatic encephalopathy
A: ICH
Hyponatraemia
Wernicke-Korsakoff
Sepsis
Drug intoxication (failure to metabolise)
Renal failure
GI bleeding

Q: Survival rate of hepatic failure?
A: <30%

Q: How does portal vein thrombosis present?
A: Acute liver failure, abdominal pain, ascites and hepatosplenomegaly

Q: What is indirect bilirubin?
A: Unconjugated

Q: What degree of LFT derangement are usually seen in alcoholic hepatitis or NASH?
A: <5x ULN

Q: In cholestatic liver enzymosis, what rises first our of AST or ALT?
A: AST before ALT

Q: What level of ALP elevation suggests cholestasis?
A: >4x ULN

Q: How much does ALP rise in pregnancy?
A: Up to 2x

Q: Half-life of albumin?
A: 3 weeks

Q: Does albumin acutely drop in fulminant liver disease?
A: No as half-life is 3 weeks but hepatic protein production drives towards immunoglobulins in infectious states

Q: Utility of HBsAg?
A: Current infection and if >6 months = chronic

Q: Utility of HBsAb
A: If high titre, suggests clearance of virus or immunisation

Q: Utility of HBcAb?
A: Previous exposure (not vaccination) but no correlation with viral activity

Q: Utility of HBeAg?
A: Recent infection and high infectivity

Q: Utility of HepB PCR?
A: Detects viral replication

Q: Ascitic tap transudate vs. exudate
A: Old: Protein <30 g/L vs. Protein >30g/L
Now use SAAG:
>11g/L = portal HTN
<11g/L = Exudative

Q: WCC and neutrophil cut-off for SBP?
A: WCC >1000/mm3 or neutrophils >250/mm3
If WCC up to 500 and predominant lymphocytes - okay
If WCC >500, highly suspect

Q: Management of mild ascites
A: Salt restrict, spironolactone 50-200mg/day and/or amiloride

Q: What proportion of patients on salt restriction + K-sparing diuretics achieve control of ascites?
A: 90%

Q: CI to ascitic tap (re: coagulation)
A: Hyperfibrinolysis as evidenced by three-dimensional bleeding, oozing from IV sites or DIC

Q: Albumin replacement dose for paracentesis
A: 6-8mg/L of fluid removed >5L
= 4% albumin 100mL per litre removed

Q: How do you differentiate SBP from secondary bacterial peritonitis?
A: SBP will have predominant neutrophils and single organism
Secondary will have predominant neutrophils, multiple organisms and 2 or more of:
 - Total protein >10g/L
 - LDH > ULN for serum
 - Glucose <5

Q: Most common bugs in SBP?
A: E. coli, Klebsiella, Strep pneumoniae

Q: Empirical treatment of SBP
A: Ceftriaxone 1g daily or PipTaz if suspect secondary bacterial peritonitis

Q: Dose of lactulose in hepatic encephalopathy
A: 30mL q1h until soft bowel motions then 3-4 times daily

Q: Enema dose of lactulose
A: 300mL in 700mL water as retained enema for 1 hour every 2 hours

Q: Which encephalopathic patients are at most risk of cerebral oedema?
A: Acute cases

Q: Which patients need hepatic coagulopathy reversed?
A: Undergoing procedure or bleeding

Q: Spotaneous recovery rate of Stage I/II hepatic encephalopathy
A: 70%

Q: Spontaneous recovery rate of Stage III hepatic encephalopathy?
A: 50%

Q: Spontaneous recovery rate of Stage IV hepatic encephalopathy?
A: <20%

Q: Which acute liver failures have the worst prognosis?
A: Age <10 or >40
Budd-Chiari
Hep B
Autoimmune hepatitis
Wilson's
Cancer
Unknown cause

Q: What are the King's college criteria for liver transplant in paracetamol-induced liver failure?
A: pH <7.3 regardless of encephalopathy
Grade III/IV encephalopathy with both PT >100 (INR >6) and creatinine >300

Q: What are the King's college criteria for liver transplant in non-paracetamol liver failure?
A: INR >6 (PT >100) OR
Encephalopathic with any 3 of:
 - Age <10 or >40
 - Bili >300
 - Time from jaundice to encephalopathy >7 days
 - Non-A, non-B or drug-induced
 - PT >50

Q: What is the modified King's college criteria for paracetamol-induced liver failure?
A: Original + Lactate >3.5 at 4 hours or pH <7.3/lactate >3 at 12 hours

Q: When should a paracetamol-induced liver failure be transferred to a transplant centre?
A: INR >3 at 48 hours or >4.5 at any time
Oliguria or creatinine >200
pH <7.3 after resus
SBP <80
Hypoglycaemia
Severe thrombocytopaenia
Encephalopathy of any degree

Q: Lifetime incidence of hernias?
A: 10%

Q: Incarcerated vs. strangulated hernia?
A: Incarcerated is stuck, strangulated is ischaemic

Q: What proportions of hernais are inguinal?
A: 75%

Q: Are the majority of inguinal hernias direct or indirect?
A: 2/3 indirect

Q: What is the most common hernia in women?
A: Inguinal

Q: What is more dangerous, direct or indirect hernia?
A: Indirect higher likelihood of strangulation/incarceration

Q: What proportion of term and pretermn infants have indirect inguinal hernias?
A: 5% of term and 30% of preterm

Q: What proportion of inguinal hernias in infants become incarcerated?
A: 15-30%

Q: Which infant inguinal hernias should be manually reduced?
A: No evidence of strangulation in boys only
(females have ovaries in them often)

Q: What proportion of patients post-laparotomy have incisional hernias?
A: Up to 20%

Q: What is the recurrence rate of incisional hernias after repair?
A: 50%

Q: Are incisional hernias at risk of incarceration?
A: Rarely

Q: In which patients are umbilical hernias most at risk of strangulation?
A: Chronic ascites - high risk of peritonitis

Q: Do umbilical hernias need to be fixed in children?
A: Usually self-resolve by age 5

Q: How much more common are femoral hernias in women?
A: 10x

Q: Management of femoral hernias?
A: Inpatient referral for repair

Q: Management of Spigelian hernia?
A: Inpatient referral for repair

Q: Management of obturator hernia?
A: Inpatient surgical repair. High risk of perforation (>50%) and mortality (20%)

Q: Steps to reduce incarcerated hernia
A: NBM
Fentanyl 1mcg/kg + Nitrous
Cold packs to hernia site
Head down
Pressure to proximal hernia neck

Q: What does MELD score predict mortality for?
A: Post-TIPS
Cirrhotic patients undergoing non-transplant surgery
Acute alcoholic hepatitis
Acute variceal haemorrhage

Q: Most common cause for lower GI bleed?
A: Upper GI bleed

Q: Most common cause of true lower GI bleeding?
A: Diverticulosis
Malignancy
Colitis
Adenomatous polyps

Q: What proportion of lower GI bleeds self-resolve?
A: 80%

Q: How often is a cause found for lower GI bleeding?
A: <50%

Q: What proportion of haematochezia is from upper GI?
A: 10%

Q: Risk factors for mesenteric ischaemia
A: AF, Age >60, CCF< recent MI, post-prandial pain, unexplained weight loss

Q: Sensitivity of CT and CT-A for mesenteric ischaemia?
A: As low as 64% and 99% respectively

Q: Mortality of ischaemic colitis
A: 50%

Q: Red flags in lower GI bleed
A: Haemodynamic instability
Repeated haematochezia
Gross blood on initial PR
Initial Hct <0.35
Syncope
Non-tender abdomen
ASpirin or NSAID use
>2 comorbidities

Q: Risk factors for aortoenteric fistula
A: Aortic graft

Q: How much bleeding is required to be seen on CT-A in GI haemorrhage?
A: >0.5mL/min

Q: Which patients with lower GI bleeding can be discharged?
A: Stable, young, obvious cause, mild bleeding only, no bright red/maroon blood on PR and without major comorbidities

Q: Extrapyramidal signs with antiemetics
A: Akathisia
Oculogyric crisis
Tardive dyskinesia
Dystonia
Parkinsonism

Q: Antidote for extrapyramidal signs of antiemetics
A: Benztropine 1mg IV slow injection

Q: Anatomic constrictions of the oesophagus
A: Cricopharyngeus C6
Aortic arch T4
GOJ T10

Q: What is transfer dysphagia?
A: Inability to transfer bolus from mouth to oesophagus
80% due to neuromuscular disorder

Q: What is transport dysphagia?
A: Impaired movement of food bolus down oesophagus
85% obstructive structural disease

Q: How does mechanical obstructive dysphagia usually progress?
A: Solids then liquids (vs. transfer dysphagia)

Q: What is Mackler's triad?
A: Chest pain, vomiting and subcut emphysema in Boerhaave'

Q: Mortality of Boerhaave's?
A: 20-90%

Q: Which objects at risk of not passing pylorus?
A: >2.5cm wide, irregular edges, sharp, >6cm long

Q: Which patients with swallowed foreign bodies need urgent endoscopy?
A: Ingestion of sharp item
Multiple FB
Button batteries in oesophagus
Evidence of perforation
Coin at level of cricopharyngeus in child
Airway compromise
Present >24 hours

Q: Which swallowed foreign bodies can be expectantly managed?
A: Distal to pylorus, benign shape, pt comfortable and tolerating oral intake

Q: Which food bolus impactions need urgent scope?
A: Complete obstruction or food with bony fragments

Q: Dose of glucagon in food impaction
A: 1mg IV q20min x 2

Q: When are repeat films required if button battery in stomach?
A: 48 hours

Q: Management of sharp objects beyond duodenum?
A: Admit
Monitor with daily AXR.
If no passage for 3 days - surgical removal
If any symptoms suggestive of perforation - surgery

Q: Mortality rate of severe pancreatitis?
A: 30%

Q: DDx of pancreatitis
A: Gallstones (50%)
Alcohol (25%)
Idiopathic
Post-ERCP
Hypertriglyceridaemia
Hypercalcaemia
Autoimmune
Infection
Tumor
Drugs

Q: Drugs that can cause pancreatitis
A: Paracetamol
Amiodarone
Carbamazepine
Oestrogens
Antiretrovirals
Azathioprine
Simvastatin
Tetracyclines
Bactrim
Dapsone
Isoniazid
Rifampicin

Q: Is pain worse lying or sitting up with pancreatitis?
A: Lying down
* Same as pericarditis

Q: How can gallstone pancreatitis be suspected on biochem?
A: ALT >150 within 48 hours of symptoms

Q: When is CT indicated in pancreatitis?
A: Diagnosis in doubt
Ranson >3
Severe clinical pancreatitis
Lack of improvement at 72 hours
Acute deterioration following initial improvement

Q: Complications of pancreatitis
A: SIRS
ARDS
DIC
AKI
Hyperglycaemia
Hypocalcaemia
Pancreatic pseudocyst
acute necrosis
Gastric outlet obstruction
Splenic/portal vein thrombosis

Q: Ranson's score components on admission
A: Age >55
WCC >16
Glucose >11
LDH >400
AST >250

Q: Indications for surgery in pancreatitis?
A: Differential diagnostic lap
Persistent biliary pancreatitis
Infected pancreatic necrosis (by FNA)
Pancreatic abscess

Q: Proportion of peptic ulcers due to H. pylori?
A: 80%

Q: Lifetime incidence of peptic ulcer disease in Western nations?
A: 10%

Q: Proportion of population colonised by H. pylori?
A: 50%

Q: Proportion of those with H. pylori that suffer peptic ulcers?
A: 10%

Q: What proportion of those with duodenal ulcers have H. pylori?
A: 90-95%

Q: What proportion of patients with gastric ulcers have H. pylori?
A: 70%

Q: Is the prevalence of H. pylori higher in those with complicated or uncomplicated duodenal ulcers?
A: Uncomplicated

Q: Who has worse outcomes from peptic/duodenal ulcers: Those with H. pylori or without?
A: Those without (especially if treated for H. pylori anyway)

Q: Do diet and alcohol cause peptic ulcer disease?
A: No

Q: What proportion of patients with dyspepsia have erosive oesophagitis?
A: 13%

Q: What proportion of those with dyspepsia have peptic ulcer disease?
A: 8%

Q: What has worse morbidity and mortality: Gastric or duodenal ulcers?
A: Gastric

Q: Classic presentation of peptic ulcer disease?
A: Burning epigastric pain, dull ache, empty feeling
Relieved by food/antacids
Recurrence when stomach empties, with recurrent pain waking at night
Tends to be daily for weeks, then resolve, then recur

Q: Red flags for dyspepsia
A: Age >50 with new symptoms
Unexplained weight loss
Persistent vomiting
Dysphagia/odynophagia
Iron deficiency anaemia
GI bleeding
Abdominal mass/lymphadenopathy
FHx of upper GI malignancy

Q: What is the rapid urease test?
A: Biopsy sample urease test
95% sensitive and specific

Q: Sensitivity and specificity of H. pylori serology?
A: Sensitivity 85%; specificity 80%

Q: Sensitivity and specificity of urease breath test?
A: 95%

Q: Sensitivity and specificity of stool antigen test for H. pylori?
A: 95%. Good test of cure after eradication therapy

Q: Who needs endoscopy for dyspepsia if no red flags?
A: If continued symptoms despite 1 month of PPI therapy
If continued symptoms despite PPI therapy + eradication of H. pylori if present

Q: When are PPI's best taken?
A: Before a meal as require acidic component to activate. Therefore work poorly if fasting or taken with H2-receptor blockers

Q: Eradication therapy for H. pylori
A: PPI + Clarithromycin + Amoxicillin for 10-14 days

Q: What proportion of peptic ulcers bleed?
A: 15% (10% mortality)

Q: DDx of post-operative fever
A: Atelectasis (first 72 hours)
Pneumonia (1-4 days)
UTI (1-5 days)
Wound (7-10 days)
DVT (> 5 days)
Drug fever
Pseudomembranous colitis

Q: Proportion of melena due to upper GI bleed?
A: 70%

Q: Increased risk of death with haematochezia from upper GI bleed?
A: x3

Q: Causes of upper GI bleed
A: Peptic ulcer 50%
Gastritis/oesophagitis 15%
Varices 10%
Mallory-Weiss 10%

Q: What proportion of upper GI bleeds in cirrhotic patients are due to varices?
A: 60%

Q: What is the most important prognostic factor in variceal haemorrhage?
A: Childs-Pugh score

Q: What proportion of those with mallory-weiss tears have history of recurrent vomiting?
A: Only 1/3

Q: What is a Dieulafoy lesion?
A: GI artery that protrudes through submucosa

Q: Indications for CXR in upper GI bleed?
A: Suspected aspiration
Co-existant cardiorespiratory disease
Suspected perforation
Elderly

Q: Do upper GI bleeders need an NG put down?
A: Can do so but risk of aspiration with placement (if not intubated), no clear benefit
No worsened outcomes if varices present
May identify blood if occult presentation but false negatives can occur if intermittent bleeding, no reflux of duodenal blood...

Q: Very low risk factors for upper GI bleed?
A: Age <60
No major comorbidities
No history of red haematemesis
No frequent melena
No haematochezia
Negative NG aspirate
Haemodynamically stable
Normal labs and Hb

Q: What does a Blatchford score of 0 indicate?
A: <1% chance of requiring intervention and therefore suitable for outpatient care

Q: Components of Blatchford score
A: Hb
BUN
SBP
Sex
HR >100
Melena
Recent syncope
Hepatic disease
CCF

Q: Low-risk Blatchford score
A: 0 [or 1 (Stanley et al.)]

Q: Components of modified Blatchford
A: Pulse, BP, BUN and Hb only. Performs as well as original

Q: Transfusion target for upper GI bleed
A: >70 OR >90 if elderly with comorbidities and not tolerating anaemia

Q: Benefits of PPI infusion in upper GI bleed?
A: Improves platelet aggregation (pH >6)
Reduces:
 - Need for surgery
 - Length of stay
 - Signs of bleeding
 - Re-bleeding
 - Blood transfusion requirement
DOES NOT improve mortality

Q: Do PPI infusions improve mortality in upper GI bleed?
A: No

Q: What proportion of patients with known varices with upper GI bleeds have an alternative source?
A: 80%

Q: Dose of octreotide in upper GI variceal bleed?
A: 50mcg IV bolus then 50mcg/hr

Q: Does octreotide improve mortality in upper GI variceal haemorrhage?
A: No. Terlipressin might (one study).
Terlipressin shown equal to octreotide for control of variceal bleeding and in-hospital survival

Q: Benefits of octreotide in variceal haemorrhage?
A: Reduces risk of persistent bleeding and rebleeding

Q: Benefits of antibiotics in variceal/cirrhotic bleeding
A: Reduces (Cochrane)
 - Infectious complications (RR 0.40)
 - All-cause mortality (RR 0.75)
 - Bacterial infection mortality (RR 0.43
 - Rebleeding (RR 0.53)
 - Length of stay (-2 days)

Q: steps of inserting Sengstaken-Blakemore or Minnesota tube
A: Intubate
Insert and confirm gastric on XR
Inflate gastric tube first with 300mL water once certain in stomach
Then inflate oesophageal tube to 50mmHg if bleeding continues
Confirm on X-ray
1L saline traction

Q: What is TIPS?
A: Transjugular intrahepatic portosystemic shunt

Q: When to transfer paracetamol intoxication to liver transplant centre?
A: INR > 3 at 48 hrs or >4.5 at any time
Oliguria or creatinine >200
pH <7.3
SBP<80
Hypoglycaemia
Severe thrombocytopenia
Encephalopathic

Q: How do you differentiate portal venous gas from pneumobilia?
A: Portal venous gas = Peripheral
Common bile duct gas = Central

Q: DDx of portal venous gas
A: NEC, ischaemic bowel, IBD, paralytic ileus, intra-abdominal sepsis

Q: DDx of pneumobilia
A: Post-instrumentation, incompetent sphincter of Oddi, Biliary-enteric surgical anastamosis, Infection (cholangitis, emphysematous cholecystitis, liver abscess)

Q: Sensitivity of USS for choledocholithiasis?
A: 60% only

Q: Sensitivity of CT for CBD stone?
A: Up to 93% if contrast enhanced and helical cholangiography protocol used

Q: Specificity of CT for choledocholithiasis?
A: 100%

Q: Which patients with haematochezia can be discharged?
A: Obvious cause and mild bleeding with haemodynamic stability

Q: Variables associated with morbidity in haematochezia
A: Haemodynamic instability
aspirin use
Non-tender abdomen
>2 comorbidities
Repeated haematochezia within 4 hours of examination

Q: What causes the majority of ischaemic colitis?
A: Non-occlusive low flow states

Q: What proportion of ischaemic colitis is non-occlusive?
A: 95%

Q: What proportion of ischaemic colitis patients suffer gangrene?
A: 15%

Q: Risk factors for ischaemic colitis
A: CPB
Aortoiliac instrumentation
MI
Haemodialysis
Thrombophilia
Constipating drugs
Vigorous exercise

Q: Three clinical stages of ischaemic colitis
A: Hyperactive phase - Severe pain, bloody stool
Paralytic phase - Diffuse more constant pain with tender distended abdo and reduced BS
Shock phase - MODS

Q: How does small bowel ischaemia present differently to large bowel?
A: More severe acute pain
More likely occlusive in nature
More likely venous occlusion
Less haematochezia

Q: Management of ischaemic colitis
A: Rule out occlusive disease on CT-A
Supportive care
Bowel rest
IV fluids
Optimise O2 and cardiac fx
Consider broad-spectrum antibiotics covering aerobes/anaerobes for moderate-severe cases to reduce bacterial translocation/sepsis risk
Admit for observation in case of gangrene

Q: Risk factors for poor outcome in ischaemic colitis
A: Male
SBP <90
HR >100
Hb <120
LDH >350
WCC >15
Na <136

Q: Benefit of PPI in upper GI bleeding?
A: Improves platelet aggregation
Reduces need for surgery
Reduces length of stay
Reduces signs of bleeding
Reduces need for intervention on endoscopy
Reduces re-bleeding
Reduces blood transfusion
DOES NOT REDUCE MORTALITY

Q: Benefits of octreotide in upper GI bleeding?
A: Reduces risk of persistent bleeding
Reduces rebleeding
DOES NOT REDUCE MORTALITY

Q: Does terlipressin reduce mortality in upper GI bleeding?
A: One study suggested it did BUT NEJM study showed equal to octreotide and no reduction in in-hospital mortality

Q: Does octreotide reduce transfusion requirements?
A: No

Q: Courvoisier's sign
A: Palpable enlarged non-tender gallbladder with jaundice = gallbladder malignancy

Q: What does bilirubin in urine suggest?
A: Conjugated hyperbilirubinaemia (also goes against biliary obstruction as cause as typically converts to urobilinogen in gut to reach urine -- although some conjugated bilirubin is soluble to enter urine)