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CST Interview > Upper GI > Flashcards

Upper GI Flashcards

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1
Q

Mx of duodenal ulcer perforation

A

Suture closure and omental patch

Treat associated H.Pylori infection with triple therapy

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2
Q

Mx of gastric ulcer perforation

A

Suture closure and mental patch if pre-pyloric

Local excision and suture closure if in body

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3
Q

Causes of Upper GI Perforation

A

Duodenal ulceration

Gastric ulceration

Gastric carcinoma

Traumatic

Ischaemia secondary to gastric volvulus

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4
Q

Treatment of gastric volvulus

A

If perforation, need sub-totel gastrectomy

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5
Q

Surgical intervention in upper GI bleed

A

Massive haemorrhage requiring on-going resus is indication for surgical management

Failed endoscopic management

Re-bleeding, not amenable to repeat endoscopic therapy

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6
Q

Risk factors for oesophageal adenocarcinoma

A

GORD

Barret’s metaplasia

Nitrosamines

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7
Q

Risk factors for oesophageal squamous cell carcinoma

A

Smoking

Alcohol

Chronic achalasia

Strictures

Reduced intake of vegetables and fruit

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8
Q

Peak age for acute appendicitis

A

Uncommon <4, >80

Peak: teens to twenties

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9
Q

Types of acute appendicitis

A

Mucosal: mildest form only identified on histopathology

Phlegmonous: slow onset, slow progression

Necrotic: often due to bacterial infection with ischaemic necrosis, leads to perforation

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10
Q

Differential diagnosis of acute appendicitis

A

Children

  • mesenteric adenitis
  • Meckel’s diverticulitis
  • Ovarian cyst
  • Menstrual

Adult
Terminal ileum: Crohn’s, Meckel’s diverticulitis
Retroperitoneal: Pancreatitis, Renal colic
Ovarian: Ectopic pregnancy, Cyst infection

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11
Q

Complications of acute appendicitis

A

Perforation

Appendix mass

Abscess

  • RIF
  • Pelvic
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12
Q

Management of acute appendicitis

A

ACUTE APPENDICITIS, i.e. not appendix mass

=open or laparoscopic appendicectomy with IV antibiotics on induction

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13
Q

Management of appendix mass or abscess

A

IV antibtiotics
-Cefuroxime 750mg TDS and Metronidazole 500mg TDS

If settles –> delayed appendicectomy

Organised abscess –> percutaneous drainage

If symptoms persist or becomes peritonitic –> appendicectomy

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14
Q

Anatonical positions of the appendix

A

Pre-ileal – anterior to the terminal ileum – 1 or 2 o’clock.

Post-ileal – posterior to the terminal ileum – 1 or 2 o’clock.

Sub-ileal – parallel with the terminal ileum – 3 o’clock.

Pelvic – descending over the pelvic brim – 5 o’clock.

Subcecal – below the cecum – 6 o’clock.

Paracecal – alongside the lateral border of the cecum – 10 o’clock.

Retrocecal – behind the cecum – 11 o’clock.

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15
Q

Blood supply to appendix

A

Lies in own mesentery with sole blood supply from the appendicular artery
-terminal branch of the iliocolic artery

Thrombosis of the appendicular artery –> gangrene

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16
Q

Open approach to appendicectomy

A

Muscle splitting gridiron at McBurney’s point

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17
Q

Causes of Acute Peritonitis

A

=inflammation of peritoneal cavity
-primary and secondary causes

Primary = very rare
e.g. streptococcal infection from blood-borne spread
Managed with extensive lavage

Secondary = common
If under 45 yrs, commonest is acute appendicitis
Acute perforated diverticular disease
Upper GI perforation 
Perforated large bowel due to malignancy 
Perforation secondary to gastric tumours
Perforated ischaemic bowel
Acute pancreatitis
Peritoneal-dialsysis related
Anastomotic leak
Enteric injury
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18
Q

Locations of intra-abdominal abscess

A

Locations

  • adjacent to offending organ
  • pelvic e.g. appendicitis
  • subphrenic e.g. upper GI perforation
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19
Q

Gynaecological causes of the acute abdomen

A

Mittelschmitz

Endometriosis

Ovarian cyst torsion

Tubo-ovarian infection / PID

Ectopic pregnancy

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20
Q

Causes of intra-abdominal abscess

A

Sigmoid diverticulitis

Acute appendicitis

Severe acute cholecystitis

Upper GI perforation

Post anastomotic leak

Infected acute pancreatitis

Post-trauma

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21
Q

Management of intra-abdominal abscess

A

IV antibiotics guided by sensitivities
IV fluids
Blood cultures

Antibiotics: e.g. Cefuroxime 750mg TDS, Metronidazole 500mg TDS

Percutaneous drainage (unless surgery needed to treat primary pathology)

Indications for surgery:

  • surgery required for primary pathology
  • failed IR drain
  • IR drain not possible e.g. retroperitoneal or intramesenteric
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22
Q

Bilirubin level for clinically apparent jaundice

A

> 40mmol

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23
Q

Causes of pre-hepatic jaundice

A

=HAEMOLYTIC

Congenital structural abnormalities

  • Hereditary spherocytosis
  • Sickle cell disease

Autoimmune haemolytic anaemia

Transfusion reactions

Drug toxicity

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24
Q

Causes of hepatic jaundice

A

Increased UNCONJUGATED

  • Gilbert’s: problem with uptake
  • Crigler-Najjar: problem with conjugation
Increased CONJUGATED
Infection
-Viral (Hep A, B, C, EBV, CMV)
-Bacterial leptospirosis or abscess
-Parasitic amoebic

Drugs

  • Paracetamol
  • Anti-psychotics
  • Antibiotics

Non-infective hepatitis

  • Alcohol
  • NAFLD
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25
Causes of post-hepatic jaundice
Intraluminal - Gallstones - Thrombus - Parasites (flukes) Mural abnormalities bile ducts - Cholangiocarcinoma - Congenital atresia - Sclerosing cholangitis - Biliary cirrhosis - Traumatic Extrinsic compression - Pancreatitis - Tumours - Lymphadenopathy - Porta hepatic node (e.g. in gastric cancer)
26
MRCP
Magnetic resonance cholangiopancreatography Indication: for extra-hepatic obstruction with no cause seen on USS
27
Complications of jaundice
Biliary infection -E. coli, Psueodomonas Coagulopathy Relative immunosuppression and decreased protein synthesis Hepatorenal syndrome
28
Management of acute obstructive gallstones
Fluid resuscitate e.g. 1000ml crystalloid Hourly UO, catheter 10mg Vitamin K for 3 days if prolonged PT IV Co-Amoxiclav ERCP
29
ERCP
Endoscopic retrograde cholangiopancreatography
30
Interventions during ERCP
Sphincterotomy - used for common bile duct stone extraction - treatment of ampullarf strictures Stent insertion - plastic (easier to remove if further intervention planned) - metal
31
Percutaneous transhepatic cholangiogram
PTC Percutaneous drainage of the biliary system
32
Choledochoduodenostomy
Communication between common bile duct and duodenum
33
Constituents of bile
Bile salts - primary: cholic, chenodeoxycholic - secondary: deoxycholic, lithocholic Phospholipids Cholesterol Increase in composition of cholesterol precipitates bile salt transformation to stones
34
Types of gallstones
Pure cholesterol - 10% - large 2.5cm stones Pure pigment - 10% - black in colour = haemolysis - brown in colour = chronic cholangitis e.g. parasites Mixed stones - 80%, by far most common - multiple in number
35
Risk factors for gallstones
Increasing age Female Pregnancy OCP Obesity Chronic haemolytic disorders Long-term parental nutrition Distal small bowel pathology e.g. Crohn's
36
Presentation of gallstones
Biliary colic Acute cholecystitis Chronic cholecystitis Mucocele Empyema
37
Symptoms and signs of biliary colic
Intermittent severe epigastric / RUQ pain Nausea & vomiting Resolves after a few hours Tenderness over gallbladder
38
Symptoms and signs of acute cholecystitis
Severe continuous RUQ pain Radiates to back / right flank Anorexia Pyrexia Tenderness over gallbladder Murphy's sign, palpation on inspiration
39
Complications of acute cholecystitis
Formation of abscess / empyema Perforation --> biliary peritonitis Cholecystoenteric fistula -> if gallstones enters and obstructs ileum = Mirizzi's syndrome
40
Mirizzi's syndrome
Type I: cholecystoenteric fistula present Type II - IV: no fistula Pathology: 1. Multiple gallstones become impacted in Hartmann's such of gallbladder 2. Leading to chronic inflammation 3. Which leads to compression of the common bile duct (CBD), necrosis, fibrosis, and ultimately fistula formation into the adjacent common hepatic duct (CHD) or common bile duct (CBD).
41
Mucocele
Stone in the neck of gallbladder Bile is absorbed BUT mucus secretions continue Forms tense globular mass in RUQ
42
Hepatobiliary iminodiacetic acid scan
Hepatobiliary iminodiacetic acid (HIDA) scan -used when USS unable to diagnose Evaluate the gallbladder. It's also used to look at the bile-excreting function of your liver and to track the flow of bile from your liver into your small intestine. A HIDA scan is often used with X-ray and ultrasound. A HIDA scan might help in the diagnosis of several diseases and conditions, such as: Gallbladder inflammation (cholecystitis) Bile duct obstruction Congenital abnormalities in the bile ducts, such as biliary atresia Postoperative complications, such as bile leaks and fistulas Assessment of liver transplant
43
Surgical management of acute cholecystitis
Cholecystectomy Indications - Symptomatic gallstones - Patients who are high-risk, with asymptomatic gallstones e. g. diabetics, pancreatitis, immunosuppression, porcelain gallbladder
44
Risks of cholecystectomy
5% are converted to open Bile duct injury <1% Bile leak 1% Bleeding 2%
45
Complications of common bile ducts stones
Obstructive jaundice Ascending cholangitis Pancreatitis
46
Presentation of common bile duct stones
Nearly always due to secondary gallstones from there gallbladder Rarely due to primary de novo stones in CBD Causes: - Obstructive jaundice - Pancreatitis - Ascending cholangitis Can be asymptomatic found on USS
47
Courvoiser's law
In a jaundice patient, a palpable gallbladder means that the diagnosis is NOT gallstones = obstructing tumour In gallstones --> small shrunken fibrotic gallbladder
48
Presentation of obstructive jaundice
Usually caused by stone in CBD Can be caused by stricture or stenosis Dark urine Pale stool Jaundice
49
Charcot's triad
Swinging fever RUQ pain Jaundice =ascending cholangitis
50
Investigations of common bile duct stones
Transabomdinal ultrasound = 1st line -low accuracy for: distal CBD stones, obese, bowel gas MRCP -if USS inconclusive ERCP -if unable to tolerate MRCP for Investigation OR -intervention required e.g. sphincterotomy and extraction or stent insertion
51
Risks of ERCP
Endoscopic retrograde cholangiopancreatography Hamorrhage Acute pancreatitis Ascending infection Perforation (retroduodenal) Risks increased with sphincterotomy
52
Indication for percutaneous transhepatic cholangiogram
in CBD stones, used when ERCP fails Risks - Sepsis - Bile leak - Tube migration - Dehydration
53
Management of CBD stones in emergency setting
Unresolving gallstone pancreatitis Ascending cholangitis Mx: ERCP sphincterotomy and stone extraction or stent Elective -previous settled complications such as pancreatitis or cholangitis, ERCP All patients scheduled for cholecystectomy for gallbladder stones should have ERCP or MRCP
54
Causes of portal hypertension
Pre-hepatic - Congenital portal vein atresia - Portal vein thrombosis - -> in neonates, secondary to umbilical sepsis - ->Intra-abdominal sepsis - Trauma - Thrombosed portocaval shunt Hepatic - Cirrhosis - Chronic hepatitis - Parasitic disease (schistosomiasis) Post-hepatic - Budd-Chiari syndrome (hepatic vein thrombosis) - Constrictive pericarditis - Tricuspid incompetence
55
Management of massive variceal bleed
A to E approach Transfuse O- negative 2 units FFP and 10mg vitamin K if iNR >1.5 Sengstaken tube, needs ITU and sedation - Gastric balloon inflated first - Traction applied, if arrests bleeding then left - If no arrest, oesophageal balloon inflated IV PPI IV Terlipressin, 4mg IV bolus Octreotide / somatostatin Endoscopic banding Transjugular intrahepatic portosystemic shunt Or Extrahepatic portocaval shunt
56
Causes of acute pancreatitis
Gallstones (60%) Alcohol (30%) Hyperlipidaemia Hypercalcaemia (multiple myeloma) Trauma: ERCP, post-surgery, cardiopulmonary bypass Toxins - Azathioprine - Oestrogens - Thiazides - Isoniazid - Steroids - NSAIDs Infection - Mumps - CMV - Hepatitis B - Mycoplasma Venom Idiopathic
57
Defining Acute Pancreatitis
Inflammatory cascade instigated by release of pancreatic enzymes trypsin, lipase, co-lipase, classically associated with a rise TNF-alpha, IL-2 and IL-6 leading to a systemic inflammatory response and multi-organ dysfunction
58
Classification of Acute Pancreatitis
Oedematous = 70% Necrotising = 25% Haemorrhagic = 5% -associated with Grey Turner's sign
59
Management of acute pancreatitis
A to E approach 1000ml plasma-lyte Catheter, strict fluid balance Low volume feeds Glascow score Consider HDU, Central line for central venous pressure, ionotropes and supportive therapy
60
Glascow Score
``` PaO2 <8kPa Age >55 years Neutrophilia >15,000 Calcium <2 Renal urea >16mmol Enzymes: ALT >200, LDH >600 Albumin <32g/L Sugar >10mmol ``` 3 or more = HDU review
61
Signs of acute pancreatitis on AXR
Sentinel loop sign Dilated proximal jejunal loop with colonic cut-off
62
Presentation of peptic ulcer disease
Peri-umbilical pain Hx of heart burn / indigestion Sudden-onset Unremitting Smoker or drinker
63
Investigations for peptic ulcer disease
``` ECG Urine dip Bloods CXR ?perforation ABG Fast scan / CT ``` ``` Mx IV plasmalyte NBM NG tube Catheter Senior r/v Boradspectrum antibiotics Theatre booking CEPOD Anaesthetist ```
64
Management of perforated peptic ulcer
NO pneumoperitoneum and NO peritonitis --> likely conservative management with IV antibiotics If acutely unwell and peritonitic --> UGRENT laparotomy Surgical: -omental graham patch repair via upper midline laparotomy
65
If recurrent ulcers despite maximal medical therapy
Consider surgical management - Highly-selective parietal cell vagotomy - Truncal vagotomy and pyelorolasty - Vagotomy and antrectomy
66
Risk factors for hypertrophic pyloric stenosis
1 month old Male > female 20% genetic
67
Presentation and signs of pyloric stenosis
Non-billous vomiting Hungry, eager to feed Dehydrated, floppy, sunken fontanelles, if delayed presentation Abnormal palpable pylorus, olive-shaped mass Distended
68
Metabolic abnormality seen in pyloric stenosis
Hypochloraemic hypokalaemic metabolic alkalosis
69
Diagnostic imaging for pyloric stenosis
Pylorus >3mm on USS Hypoechoic ring
70
Management of pylorus stenosis
Paediatric ALS IV /IO access 20ml/kg fluid bolus Ramstedt pyloromyotomy -circumumbilical incision Resume feeding 12 - 24 hours post op

CST Interview (11 decks)

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