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CST Interview > Upper GI > Flashcards

Upper GI Flashcards

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
Q

Causes of post-hepatic jaundice

A

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)
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26
Q

MRCP

A

Magnetic resonance cholangiopancreatography

Indication: for extra-hepatic obstruction with no cause seen on USS

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27
Q

Complications of jaundice

A

Biliary infection
-E. coli, Psueodomonas

Coagulopathy

Relative immunosuppression and decreased protein synthesis

Hepatorenal syndrome

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28
Q

Management of acute obstructive gallstones

A

Fluid resuscitate e.g. 1000ml crystalloid
Hourly UO, catheter
10mg Vitamin K for 3 days if prolonged PT
IV Co-Amoxiclav
ERCP

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29
Q

ERCP

A

Endoscopic retrograde cholangiopancreatography

30
Q

Interventions during ERCP

A

Sphincterotomy

  • used for common bile duct stone extraction
  • treatment of ampullarf strictures

Stent insertion

  • plastic (easier to remove if further intervention planned)
  • metal
31
Q

Percutaneous transhepatic cholangiogram

A

PTC

Percutaneous drainage of the biliary system

32
Q

Choledochoduodenostomy

A

Communication between common bile duct and duodenum

33
Q

Constituents of bile

A

Bile salts

  • primary: cholic, chenodeoxycholic
  • secondary: deoxycholic, lithocholic

Phospholipids

Cholesterol

Increase in composition of cholesterol precipitates bile salt transformation to stones

34
Q

Types of gallstones

A

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
Q

Risk factors for gallstones

A

Increasing age

Female

Pregnancy

OCP

Obesity

Chronic haemolytic disorders

Long-term parental nutrition

Distal small bowel pathology e.g. Crohn’s

36
Q

Presentation of gallstones

A

Biliary colic

Acute cholecystitis

Chronic cholecystitis

Mucocele

Empyema

37
Q

Symptoms and signs of biliary colic

A

Intermittent severe epigastric / RUQ pain

Nausea & vomiting

Resolves after a few hours

Tenderness over gallbladder

38
Q

Symptoms and signs of acute cholecystitis

A

Severe continuous RUQ pain

Radiates to back / right flank

Anorexia

Pyrexia

Tenderness over gallbladder

Murphy’s sign, palpation on inspiration

39
Q

Complications of acute cholecystitis

A

Formation of abscess / empyema

Perforation –> biliary peritonitis

Cholecystoenteric fistula
-> if gallstones enters and obstructs ileum = Mirizzi’s syndrome

40
Q

Mirizzi’s syndrome

A

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
Q

Mucocele

A

Stone in the neck of gallbladder

Bile is absorbed BUT mucus secretions continue

Forms tense globular mass in RUQ

42
Q

Hepatobiliary iminodiacetic acid scan

A

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
Q

Surgical management of acute cholecystitis

A

Cholecystectomy

Indications

  • Symptomatic gallstones
  • Patients who are high-risk, with asymptomatic gallstones
    e. g. diabetics, pancreatitis, immunosuppression, porcelain gallbladder
44
Q

Risks of cholecystectomy

A

5% are converted to open

Bile duct injury <1%

Bile leak 1%

Bleeding 2%

45
Q

Complications of common bile ducts stones

A

Obstructive jaundice

Ascending cholangitis

Pancreatitis

46
Q

Presentation of common bile duct stones

A

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
Q

Courvoiser’s law

A

In a jaundice patient, a palpable gallbladder means that the diagnosis is NOT gallstones
= obstructing tumour

In gallstones –> small shrunken fibrotic gallbladder

48
Q

Presentation of obstructive jaundice

A

Usually caused by stone in CBD
Can be caused by stricture or stenosis

Dark urine
Pale stool
Jaundice

49
Q

Charcot’s triad

A

Swinging fever

RUQ pain

Jaundice

=ascending cholangitis

50
Q

Investigations of common bile duct stones

A

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
Q

Risks of ERCP

A

Endoscopic retrograde cholangiopancreatography

Hamorrhage
Acute pancreatitis
Ascending infection
Perforation (retroduodenal)

Risks increased with sphincterotomy

52
Q

Indication for percutaneous transhepatic cholangiogram

A

in CBD stones, used when ERCP fails

Risks

  • Sepsis
  • Bile leak
  • Tube migration
  • Dehydration
53
Q

Management of CBD stones in emergency setting

A

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
Q

Causes of portal hypertension

A

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
Q

Management of massive variceal bleed

A

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
Q

Causes of acute pancreatitis

A

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
Q

Defining Acute Pancreatitis

A

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
Q

Classification of Acute Pancreatitis

A

Oedematous = 70%

Necrotising = 25%

Haemorrhagic = 5%
-associated with Grey Turner’s sign

59
Q

Management of acute pancreatitis

A

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
Q

Glascow Score

A 
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
Q

Signs of acute pancreatitis on AXR

A

Sentinel loop sign

Dilated proximal jejunal loop with colonic cut-off

62
Q

Presentation of peptic ulcer disease

A

Peri-umbilical pain

Hx of heart burn / indigestion

Sudden-onset

Unremitting

Smoker or drinker

63
Q

Investigations for peptic ulcer disease

A 
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
Q

Management of perforated peptic ulcer

A

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
Q

If recurrent ulcers despite maximal medical therapy

A

Consider surgical management

  • Highly-selective parietal cell vagotomy
  • Truncal vagotomy and pyelorolasty
  • Vagotomy and antrectomy
66
Q

Risk factors for hypertrophic pyloric stenosis

A

1 month old

Male > female

20% genetic

67
Q

Presentation and signs of pyloric stenosis

A

Non-billous vomiting

Hungry, eager to feed

Dehydrated, floppy, sunken fontanelles, if delayed presentation

Abnormal palpable pylorus, olive-shaped mass

Distended

68
Q

Metabolic abnormality seen in pyloric stenosis

A

Hypochloraemic hypokalaemic metabolic alkalosis

69
Q

Diagnostic imaging for pyloric stenosis

A

Pylorus >3mm on USS

Hypoechoic ring

70
Q

Management of pylorus stenosis

A

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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