GI - Peptic ulcer, Gallstones, Pancreatitis Flashcards

Question

Clinical features of peptic ulcer Differentiating S/S between gastric ulcer and duodenal ulcers

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

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

Answer 6

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

Answer 7

→ 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

Answer 8

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)

Answer 9

→ 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

Answer 10

1. Cholesterol - cholesterol monohydrate crystals; Yellow, fine granular, hard, faceted 2. Black Pigmented - calcium bilirubinate; Jet-black, hard, speculated and brittle 3. Brown Pigmented - calcium bilirubinate, palmitate, sterate with dead bacteria; Brown, softer, clay-like 4. Mixed (majority) - both cholesterol and calcium salts; ‘egg-shell’ appearance on plain XR films

Answer 11

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

Answer 12

"Fat + Female + Fertile + Forty" 1. Excessive cholesterol secretion - Hormonal: multiparity, OCP - Metabolic: obesity, DM, ↑lipids 2. Gallbladder stasis - ↓enteric intake: aggressive weight reduction, NPO on TPN - Neurogenic: SCI, truncal vagotomy - Hormonal: pregnancy, OCP, HRT

Answer 13

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 2. Bile acid malabsorption Ileal disease: resection, Crohn’s disease 3. GB stasis

Answer 14

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: 1. Bacterial infection of biliary tree 2. Strictures: parasitic-induced (RPC), prior ERCP strictures, malignancy 3. Other causes, eg. stents

Answer 15

Prior cholesterol stone causes stasis and bacterial colonization → deconjugation of bilirubin forming calcium bilirubinate component on top of cholesterol stone

Answer 16

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

Answer 17

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

Answer 18

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

Answer 19

Asymptomatic gallstones Symptomatic or complicated gallstones risk of CA gallbladder, eg. GB polyp >0.5cm, porcelain gallbladder

Answer 20

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

Answer 21

→ Neoplasm: pancreatic or ampullary tumour → Congenital: pancreas divisum, choledochocele type V → Genetics, eg. cystic fibrosis, PRSS1, SPINK1 and other mutations

Answer 22

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

Answer 23

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

Answer 24

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

Answer 25

→ Cullen’s sign: bruises of periumbilical region → Grey Turner’s sign: bruises of flank region → Fox’s sign: bruises over inguinal ligament

Answer 26

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

Answer 27

≥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

Answer 28

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

Answer 29

TAUS shows: → Focal or diffuse enlargement with homogeneous enhancement → Peripancreatic fat stranding → ± complications: necrosis, abscesses...etc

Answer 30

Peptic ulcer disease Perforated Peptic ulcer Cholangitis, CBD gallstones Cholecystitis Intestinal obstruction Mesenteric ischemia

Answer 31

``` 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 ```

Answer 32

Mortality: 0-2% (0-2), 15% (3-4), 50% (5-6), 70-90% (≥7)

Answer 33

1. IV fluid resuscitation 2. NPO + NGT aspiration if persistent vomiting, significant gastroparesis or ileus 3. Enteral feeding/ Parenteral feeding 4. Analgesics: Opioids: preferred, usually fentanyl, hydromorphone, tramadol, NOT MORPHINE (tighten sphincter of Oddi) 5. Antibiotics: therapeutic (NOT prophylactic) for infected necrosis 6. Serial contrast CT

Answer 34

1. Infected necrosis: empirical antibiotics and percutaneous drainage/ endoscopic debridement 2. Bowel ischemia, acute necrotizing cholecystitis, ongoing bleed: surgical debridement/ necrosectomy 2. ERCP for biliary stone removal 3. Manage complications or organ failures

Answer 35

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) ```

Answer 36

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

Answer 37

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

Answer 38

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 ```

Answer 39

CA pancreas □ Clinical features: older age, absence of Hx of alcohol use, weight loss, protracted flare of Sx, significant constitutional symptoms

Answer 40

1. Lifestyle modifications: Abstinence from alcohol Small low-fat meals with hydration/ fat-restricitons Cessation of smoking 2. Pain relief: Analgesics: opioids, low-dose amitriptyline + NSAIDs 3. Oral pancreatic enzyme supplements, eg. pancreatin 4. Endoscopic dilatation of ductal strictures/ Surgical drainage/ resection e.g. Whipple’s procedure 5. Medium-chain triglycerides (MCTs) + Vitamin supplementation: vitamin D, calcium 6. Insulin for secondary DM

Answer 41

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

Answer 42

→ 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