GI - Peptic ulcer, Gallstones, Pancreatitis Flashcards
Ddx GI causes of epigastric pain
Gastroduodenal
- Peptic ulcer
- Atypical GERD
- Gastric cancer
Hepatobiliary:
- Pancreatitis
- Gallstones
- Pancreatic cancer
Functional dyspepsia (*60%)
Ddx non-GI causes of epigastric pain
Cardiac: MI, myocarditis, ACS…etc
Chest: Pneumothorax, PE…etc
Haematological: Acute leukaemia, hemolytic anaemia..etc
Metabolic: Uremia, DM, porphyria, Addision’s
Toxin: lead poisoning, hypersensitivity
Infections: Herpes zoster (shingles)
Neurological: radiculitis, tabes dorsalis
Misc: muscular contusion, narcotic withdrawal, psychiatric disorders..etc
Differentiate the likely organs involved in constant vs Colicky vs episodic/ plateau epigastric pain
Constant moderate pain - likely ulcers
Colicky - likely intestinal or renal colic
Episodic/ plateau - likely biliary colic/ pancreatic pain
Ddx acute epigastric pain radiating to back
Biliary pain
Acute pancreatitis
Dissecting aortic aneurysm
Posteriorly penetrating PU
Ddx epigastric pain with repeated vomiting
Food poisoning/ gastroenteritis
Acute pancreatitis
Gastric outlet obstruction
Ddx agonizing, generalized abdominal pain
Mesenteric thrombosis
Ischemic colitis
Peritonitis
Perforated acute pancreatitis
Alarming features of acute epigastric pain
Age: >45 years old
Constitutional symptoms: Anaemia/ bleeding, Unintentional weight loss, Anorexia, lymphadenopathy
Alarming S/S
- Early satiety
- Abdominal mass
- Jaundice
- Dysphagia or odynophagia
- Persistent vomiting
PMH:
- Upper GI cancer
- Ulcers
Family history: upper GI cancer
Peptic ulcers
- Specify possible locations of ulceration
Gastric ulcer (20%) - usu. at lesser curvature and corpus-antrum junction
Duodenal ulcer (75%) - usu. solitary D1 if no NSAID use
Esophageal ulcer
Merkel’s diverticulum (ectopic epithelium)
Anastomotic ulcer/ Stoma opening (gastroenterostomy)
Peptic ulcer complications and S/S
Ulcer complications: ‘bleed’, ‘burst’, ‘block’ and ‘burrow’ (fistulization to other organs)
→ Bleeding: symptomatic UGIB, anaemia
→ Perforation: abrupt severe epigastric pain secondarily generalized, fever, shock
→ Gastric outlet obstruciton: nausea, vomiting (of old food >1h), epigastric distension
Peptic ulcer
- Aetiologies
H. pylori infection: 92% DU, 70% GU
NSAIDs: 5% DU, 25% GU
Stress, ICU setting esp if mechanical ventilation or coagulopathy
Zollinger-Ellison syndrome (gastrinoma, G cell hyperplasia)
→ Features: hypergastrinaemia + ulcers at atypical location
Smoking
Drugs: alcohol, antiplatelets, steroids
Crohn’s Disease
Pathogenesis of stress peptic ulcers
Stress ulcers are due to biliary reflux, uraemic toxins and impaired perfusion to stomach, leading to impairment of mucosal protection of stomach
H. pylori
- Pathophysiology of gastric mucosa inflammation
Pathology: Expresses certain cytotoxins to provoke gastritis in underlying epithelium
Antral gastritis (majority) → ↓somatostatin, ↑gastrin release → ↑acid production → DU ± GU
Pangastritis (minority, 1%) → chronic atrophic gastritis ± GU → hypochlorhydria → proliferation of other bacteria → mutagenic nitrites → ↑risk of CA stomach
H.pylori
- Gram stain, morphology
- Survival mechanism in stomach
- Transmission
- Risk factors of infection
Bacteriology: G- bacilli, spiral w/ unipolar flagella
→ Resides in mucus layer overlying mucosa where pH is~7
→ Expresses urease to convert urea into ammonia + bicarbonate → counteract stomach acidity
Transmission: unknown, likely person-to-person contact via oro-oral or feco-oral route
RFs: unclean water supply, poor sanitary conditions, crowded environment, ↓socio-economic status
H. pylori-associated diseases
Dyspepsia, chronic gastritis, PUD (GU/DU) Gastric adenocarcinoma, MALT lymphoma Extra-GI: anaemia (due to B12 or Fe def)
Diagnostic tests for H. pylori infection
Which tests used for post-treatment monitoring
Invasive endoscopic tests: 3 biopsies at antrum/ proximal stomach
- Rapid urease test (CLO test)
- Biopsy for histology
- Culture for S/T
Non-invasive: Whole blood/ serum test for antibodies (Specific IgG) Urine antibody Stool antigen Urea breath test with C-13 isotope
Stool antigen and urea breath test are used for post-treatment monitoring
Mechanism of rapid urease test/ CLO test
Rapid urease test (CLO test): sens 90%, spec 95%
→ Bx sample added to a solution of urea + phenol red
→ urease-positive H. pylori will hydrolyze urea into NH3 + CO2
→ ↑pH turns phenol red from yellow to pink
→ usually read at 1h and 4h (85% will change colour ≤1h)
Treatment regimens of H. pylori infection
Triple therapy: PPI + amoxicillin + clarithromycin bi-daily ×7d
Bismuth quadruple therapy: PPI + bismuth + tetracycline + metronidazole
Non-bismuth quadruple therapy: PPI + amoxicillin + clarithromycin + Metronidazole
Indication for Bismuth-containing quadruple therapy
Dual clarithromycin and metronidazole resistance (>15%)
Post H pylori treatment monitoring
NON-invasive tests, eg. stool antigen tests, urea breath tests
Pathogenesis of NSAID-related peptic ulcer
Pathology:
Impair gastric mucosa defense:
- Block prostaglandin production
- Block bi-carbonate and mucus production
> > Impair mucus layer, lowers pH and increase susceptibility of gastric acid and pepsin attack
pH dependent gastric mucosal damage
NSAID-related peptic ulcer
Risk factors: patient factors and drug factors
Patient factors:
- Age >60y
- Hx of PUD or UGI complications
Drug-related factors:
- ↑COX-1 selectivity
- High dose or concurrent use
- Concurrent anticoagulants or steroids
Which NSAIDs cause most peptic ulcer
Which cause the least
Most PU:
Aspirin, Ketoprofen, Etodolac, Piroxicam
Least PU:
Fenoprofen, Diclofenac, Naproxen
Prevention of NSAID-related peptic ulcer
Prevention:
→ Review meds: review indications for NSAIDs, consider switching to less ulcerogenic NSAIDs or COX-2 inhibitor
→ Prior H. pylori testing ± eradication
→ Co-therapy by PPI, H2 receptor antagonist, misoprostol (Prostaglandin analogue)
Prevention of aspirin related GI complications
H. pylori eradication
H2 receptor antagonist, PPI, Misoprostol use
Substitute aspirin with Clopidogrel
Clinical features of peptic ulcer
Differentiating S/S between gastric ulcer and duodenal ulcers
Dyspepsia (80%): variable discomfort at epigastrium ± radiation
- ulcer-like (burning/gnawing pain) or
- dysmotility-like (bloating, early satiety, anorexia, nausea)
Pain localizes to epigastrium, related to food and episodic
GU vs DU:
- GU is exacerbated by eating vs DU relieved by eating → corresponding weight changes
- DU a/w pain at night and 2-3 hours after eating vs GU pain during eating
Diagnostic investigations of peptic ulcer disease
Management plan of uncomplicated PUD
OGD with biopsy:
- Diagnotic: Biopsy to confirm PUD, r/o malignancy, H. pylori testing
- Therapeutic: stop ulcer bleeding
Mx of underlying cause:
→ H. pylori eradication therapy as above
→ Avoid NSAIDs, stop smoking and limit alcohol intake
Antisecretory therapy: PPI
Re-scope at 6mo for GU to detect non-healing ulcers
Management plan of refractory/ complicated PUD
Surgical therapy for refractory or complicated ulcers: lower risk of malignancy
→ GU: ulcer excision, eg. partial gastrectomy + Bilroth I (or II) reconstruction
→ DU: acid-reducing procedures, eg. truncal vagotomy + pyloroplasty
Management of urgent peptic ulcer bleeding
IV PPI: bolus + maintenance → mandatory for any UGIB
Endoscopic Treatments: e.g. hemoclip, heater probe…etc
Angiography for transcatheter arterial embolization (TAE)
Surgical Mx:
- DU: duodenotomy with 3-point ligation of gastroduodenal a.
- GU: plication + Bx vs partial gastrectomy + B1/2 reconstruction
Presentation of perforated PU
S/S: triad of
→ Sudden abdominal pain:
- Epigastric onset, secondarily generalized
- ± radiation to shoulder tip (diaphragm irritation) and RLQ (spillage into paracolic gutter)
→ ‘Board-like’ rigidity due to generalized peritonitis
- Absent bowel sounds
- ↓liver dullness due to free gas under diaphragm
→ Systemic upset: tachycardia, fever, tachypnoea, septic/hypovolemic shock
Investigations to confirm perforated PU
Pneumoperitoneum on imaging:
- Erect CXR: free gas under peritoneum (≥50%) ± continuous diaphragm sign
- AXR: ↑clarity of organ outlines,
eg. double wall sign (Rigler sign) eg. falciform ligament sign eg. urachus sign eg. hepatic edge sign - USG for peritoneal stripe sign
- CT for free gas or fluid in peritoneal cavity
Management of perforated PU
→ Prompt resuscitation + NPO + NGT suction
→ IV broad spectrum Abx, PPI and analgesics
→ Urgent OT:
- GU: direct repair in young (↓risk of CA), partial gastrectomy + reconstruction in old
- DU: omental patch repair60 ± acid-reducing procedure
→ Post-op eradication of cause, eg. PPI, HP eradication, NSAID avoidance
Ulcer-related gastric outlet obstruction
Pathogenesis
S/S
Dx
Pathogenesis:
spasm, oedema, pyloric dysmotility due to acute inflammation + fibrosis due to chronic inf’n
» gastric atony after prolonged GOO
S/S:
→ Early satiety, bloating, indigestion, anorexia, weight loss
→ Nausea, vomiting (large quantities, characteristically of content 8-12h after eating)
→ Epigastric distension w/ succussion splash or visible peristalsis after eating
→ Electrolyte disturbance: dehydration (↑urea), hypoK, hypoCl metabolic alkalosis
Approach:
→ Resuscitation + correction of electrolytes + NGT suction
→ OGD: Bx for underlying pathology (esp to exclude malignancy)
Gallstones
- Define terms for stone in gallbladder, CBD, intrahepatic ducts
- Define complicated vs uncomplicated gallstones disease
→ Cholecystolithiasis: stone in gallbladder
→ Choledocholithiasis: stone in the common bile duct
→ Hepatolithiasis: stones in intrahepatic bile ducts (i.e. RPC)
→ Uncomplicated gallstone disease: biliary colic w/o gallstone-related complications
→ Complicated gallstone ds: a/w gallstone-related complications, eg. acute cholecystitis, cholangitis, gallstone pancreatitis, gallstone ileus, Mirizzi syndrome
List 4 major types of gallstones, appearance and respective composition
- Cholesterol - cholesterol monohydrate crystals; Yellow, fine granular, hard, faceted
- Black Pigmented - calcium bilirubinate; Jet-black, hard, speculated and brittle
- Brown Pigmented - calcium bilirubinate, palmitate, sterate with dead bacteria; Brown, softer, clay-like
- Mixed (majority) - both cholesterol and calcium salts; ‘egg-shell’ appearance on plain XR films
Pathogenesis of cholesterol gallstones
Liver secretes cholesterol in vesicular form with phospholipids
→ dissolved in GB by bile salts into micelles
→ GB concentration of bile results in overwhelming of dissolving capacity of bile salts
→ supersaturation and crystallization
Risk factors of cholesterol gallstones
“Fat + Female + Fertile + Forty”
- Excessive cholesterol secretion
- Hormonal: multiparity, OCP
- Metabolic: obesity, DM, ↑lipids - Gallbladder stasis
- ↓enteric intake: aggressive weight reduction, NPO on TPN
- Neurogenic: SCI, truncal vagotomy
- Hormonal: pregnancy, OCP, HRT
Pathogenesis of black pigmented gallstones
Risk factors
Stone formation requires unconjugated bilirubin which can come from
(1) spillage from ↑haeme turnover [cause of black stones]
(2) bile acid malabsorption
Risk factors:
1. ↑haeme turnover
Haemolysis: G6PD (commonest), cirrhosis-related hypersplenism, thalassaemia
Gilbert syndrome
- Bile acid malabsorption
Ileal disease: resection, Crohn’s disease - GB stasis
Pathogenesis of brown pigmented gallstones
Risk factors
Unconjugated bilirubin is formed within an infected biliary tree where there is bacterial β-glucuronidase
Bacteria also hydrolyze phospoholipids to release FAs from fat vesicles → form calcium salts → accounts for softer texture
Risk factors:
- Bacterial infection of biliary tree
- Strictures: parasitic-induced (RPC), prior ERCP strictures, malignancy
- Other causes, eg. stents
Pathogenesis of mixed gallstone
Prior cholesterol stone causes stasis and bacterial colonization
→ deconjugation of bilirubin forming calcium bilirubinate component on top of cholesterol stone
Four stages of gallstone disease
Gallstone disease
- Typical presentation
- Complications
Typical presentation
- Mostly asymptomatic, incidental finding
- Biliary colic, nausea, vomiting, dyspepsia, fat intolerance
Complications:
GB: cholecystitis (± gangrene, empyema, perforation), CA GB, Mirizzi syndrome
CBD: CBD stone, cholangitis
Others: gallstone pancreatitis, gallstone ileus, pancreatitis
Gallstone disease
- Pathophysiology of biliary colic
- S/S (OPQRST)
Pathogenesis: impaction of gallstones or sludge in cystic duct during GB contraction → pain due to GB distension
stereotypical attacks of upper abd pain after ingestion of fatty meal
- Onset: begins quite suddenly and increases steadily over 10-20min
- Precipitation: usually begins post-prandially, or at night
- Quality: intense, dull pain
- Region/radiation: occurs in epigastric region initially and may migrate to RUQ; may radiate to right scapular tip (Collin’s sign)
- Severity: intense, waxing-and-waning
- Timing: usually lasts 1-5h
First-line investigations for gallstones
P/E + blood tests: should be normal
AXR: for pigmented stones (cannot see cholesterol stones)
Trans-abdominal US**
- Stones: echogenic foci that casts an acoustic shadow
- Sludge: heterogenous enhancement w/o shadow
ERCP/PTBD: usually for therapeutic purposes
Additional:
EUS ± bile collection: identify small stones missed on TAUS esp CBD ones
MRCP: usually as 2nd line if TAUS -ve
Indications for cholecystectomy
Asymptomatic gallstones
Symptomatic or complicated gallstones
risk of CA gallbladder, eg. GB polyp >0.5cm, porcelain gallbladder
Causes of acute pancreatitis
Idiopathic (15-25%)
Gallstones (55%)
Ethanol (35%): acute exacerbation of chronic alcoholism
Trauma
Steroids: ↑viscosity of pancreatic juice
Mumps and other infections:
→ Viruses: mumps, coxsackievirus, hepatitis B, CMV, VZV, HSV, HIV
→ Bacterial: Mycoplasma, Legionella, Leptospira, Salmonella
→ Fungal: Aspergillus
→ Parasitic: Toxoplasma, Cryptosporidium, Ascaris
Autoimmune: SLE, Sjogren’s syndrome, vasculitis (eg. PAN)
Scorpion/ toxins, eg. organophosphate poisoning (cholinergic stimulation)
Hypercalcaemia (3rd commonest) and Hypertriglyceridaemia (4th)
ERCP-related (2-5%)
Drugs (1-2%), eg. Sulphamethoxazole-trimethoprim, Azathioprine, NSAIDs, Diuretic, valproate
Neoplastic, congenital and genetic causes of acute pancreatitis
→ Neoplasm: pancreatic or ampullary tumour
→ Congenital: pancreas divisum, choledochocele type V
→ Genetics, eg. cystic fibrosis, PRSS1, SPINK1 and other mutations
Pathogenesis of acute pancreatitis
Inciting event = acinar cell injury leading to premature trypsinogen activation within acina + inflammation
→ Ductal obstruction (eg. gallstones) → interstitial oedema → impaired blood flow → acinar cell injury
→ Acinar cell injury (eg. alcohol, drugs, hyperCa) → ↑inappropriate intracellular release + activation of enzymes
→ Defective intracellular transport
Acute Pancreatitis:
Local histological changes
Systemic responses
Progression
Early local changes:
→ Autodigestion of pancreatic tissues, fat necrosis
→ Microcirculatory injury: interstitial oedema and ischaemia-reperfusion injury
→ Inflammatory changes (esp NFκB activation) with cytokine release and leukocyte activation
Systemic responses:
SIRS due to systemic spillage of cytokines and activated pancreatic enzymes
Bacterial translocation: systemic hypovolemia + gut A-V shunting, systemic sepsis with endotoxaemia
Progression:
Necrotizing pancreatitis: persistent ampullary obstruction + hypoperfusion
Acute pancreatitis
Clinical presentation (OPQRST) + associated S/S
Severe epigastric pain that radiates to the back
→ Acute onset, of increasing intensity over 15-60min, lasts for several hours to days
→ Severe, constant, boring sensation that radiates to the back (50%)
→ Usually localized to upper abdomen, occ. in RUQ or rarely LUQ
→ Usually ↑ by movement and ↓by sitting up and leading forward
→ Initially a/w very little peritoneal signs
Associated S/S
□ Nausea and vomiting (90%)
□ Fever
□ Features of retroperitoneal haemorrhage
List Features of retroperitoneal haemorrhage in haemorrhagic pancreatitis
→ Cullen’s sign: bruises of periumbilical region
→ Grey Turner’s sign: bruises of flank region
→ Fox’s sign: bruises over inguinal ligament
Complications and S/S of acute pancreatitis
Diffuse peritonitis
Hypovolaemia ± shock
Dyspnoea: due to pleural effusion or ARDS
Palpable pseudocyst
Pancreatic ascites when fluid leaks from disrupted pancreatic duct into peritoneal cavity
Splanchnic venous thrombosis
Abdominal compartment syndrome due to tissue oedema, ascites, ileus
Diagnostic criteria of acute pancreatitis
≥2 out of 3 of (Revised Atlanta classification, 2013)
□ Epigastric pain: acute onset of persistent, severe epigastric pain often radiating to the back
□ ↑serum lipase/amylase to ≥3× ULN
□ Characteristic imaging finding of acute pancreatitis on contrast CT, MRI or trans-abdominal USG
First-line investigations of acute pancreatitis
LFT: high ALT for gallstone pancreatitis, high bilirubin for gallstone at ampulla
Abdominal ultrasound: Swollen pancreas, Peripancreatic fluid anechoic collection
Endoscopic US: occult biliary stones
ERCP for gallstone clearance
Serum amylase
Serum Ca, lipids → hyperCa, hyperlipidaemia
CXR: mainly to r/o PPU, complications like pleural effusions or ARDS
AXR: focal ileus with sentinel loop sign, or calcification of chronic pancreatitis
Contrast CT to confirm diagnosis and find cause later
Indications for additional Contrast CT for acute pancreatitis
TAUS shows:
→ Focal or diffuse enlargement with homogeneous enhancement
→ Peripancreatic fat stranding
→ ± complications: necrosis, abscesses…etc
D/dx acute pancreatitis
Peptic ulcer disease
Perforated Peptic ulcer
Cholangitis, CBD gallstones
Cholecystitis
Intestinal obstruction
Mesenteric ischemia
Severity score for acute pancreatitis
Glasgow’s criteria: ≥3 within first 48h indicates a severe attack □ PaO2: <8kPa = 60mmHg □ Age: >55 years □ Neutrophils: >15× 109/L □ Calcium: <2mmol/L □ Renal: urea >16mmol/L □ Enzymes: LDH >600IU/L or AST/ALT >200IU/L □ Albumin: <32g/L □ Sugar: glucose >10mmol/L
Outline the Atlanta classification for severity/ complications of acute pancreatitis
Severity/ Mortality score for acute pancreatitis
Mortality: 0-2% (0-2), 15% (3-4), 50% (5-6), 70-90% (≥7)
Supportive treatment for mild acute pancreatitis
- IV fluid resuscitation
- NPO + NGT aspiration if persistent vomiting, significant gastroparesis or ileus
- Enteral feeding/ Parenteral feeding
- Analgesics: Opioids: preferred, usually fentanyl, hydromorphone, tramadol, NOT MORPHINE (tighten sphincter of Oddi)
- Antibiotics: therapeutic (NOT prophylactic) for infected necrosis
- Serial contrast CT
Definitive treatment for severe acute pancreatitis
- Infected necrosis: empirical antibiotics and percutaneous drainage/ endoscopic debridement
- Bowel ischemia, acute necrotizing cholecystitis, ongoing bleed: surgical debridement/ necrosectomy
- ERCP for biliary stone removal
- Manage complications or organ failures
Chronic pancreatitis
Pathogenesis
Causes
Chronic pancreatitis: prolonged inflammation of pancreas a/w irreversible destruction of exocrine parenchyma, fibrosis and, in late stages, destruction of endocrine parenchyma
Aetiology: NOT gallstones - Alcohol - Toxic-metabolic: tobacco smoking, hyperCa, chronic renal failure - Severe, recurrent acute pancreatitis - Autoimmune: IgG4-related disease - Ductal obstruction (genetics and congenital...etc)
Chronic pancreatitis
Clinical presentation
Abdominal pain
- Epigastric with radiation to back
- Worse post-prandial
- Improve by sitting forward, drink alcohol
Pancreatic exocrine insufficiency (90% exocrine mass loss)
- Fat malabsorption: steatorrhoea ± vitamin A, D, E, K, B12 malabsorption
- Protein malabsorption
Pancreatic endocrine insufficiency, i.e. secondary diabetes mellitus
Loss of weight: 2o to combination of anorexia, avoidance of food (post-prandial discomfort) and DM
Chronic pancreatitis
Physical findings
Weight loss: thin, malnourished
Epigastric tenderness
Enlarged pancreas: occ. palpable, esp in thin pt (d/dx pseudocyst)
Erythema ab igne: skin pigmentation over abdomen/back
First-line investigations for chronic pancreatitis
Radiological diagnosis: usually 1st line:
Plain AXR: calcifications in pancreatic duct
USG: ductal dilatation, parenchymal changes with ↑echogenicity and irregular gland contour
CT: ductal dilatation, calcification, pseudocysts
EUS
ERCP: current gold-standard: Characteristic chain-of-lakes appearance of ductal anatomy
Biochemical: Faecal pancreatic elastase Secretin stimulation test 72h fecal fat collection OGTT for endocrine insufficiency
Major ddx of chronic pancreatitis
CA pancreas
□ Clinical features: older age, absence of Hx of alcohol use, weight loss, protracted flare of Sx, significant constitutional symptoms
Treatment plan of chronic pancreatitis
- Lifestyle modifications:
Abstinence from alcohol
Small low-fat meals with hydration/ fat-restricitons
Cessation of smoking - Pain relief:
Analgesics: opioids, low-dose amitriptyline + NSAIDs - Oral pancreatic enzyme supplements, eg. pancreatin
- Endoscopic dilatation of ductal strictures/ Surgical drainage/ resection e.g. Whipple’s procedure
- Medium-chain triglycerides (MCTs) + Vitamin supplementation: vitamin D, calcium
- Insulin for secondary DM
Complications of chronic pancreatitis
Pseudocyst formation (10%)
CBD/duodenal obstruction (5-10%): inflammation and fibrosis of HOP or pseudocyst
Pancreatic ascites and pleural effusion/ fistulation into peritoneal/pleural cavity
Splenic vein thrombosis (11%)
CA pancreas
Ddx perforated PU
→ SB: perforated diverticulum, SB ulcer (eg. CMV), tumours (lymphoma (most common), CA lung and breast)
→ LB: closed loop obstruction, diverticulum
→ Acute appendicitis: NO GAS because of obstruction
→ Others: colonoscopy-related, FB-related
