Upper GI Flashcards
What organism can cause dyspepsia and how do we test for it? What two classes of medications do we use to treat dyspepsia? If left untreated, there is increased risk of what? (Formative Q)
- Helicobactor pylori which is most commonly detected using a stool antigen test before initiation of treatment.
- H2 blockers such as ranitidine and proton pump inhibitors (PPIs) such as omeprazole.
- Gastric, duodenal cancer
Barrett’s Oesophagus - pathophysiology, RF, Presentations, Ix,Mx, Complications
(1. ) Normal stratified squamous epithelial replaced by metaplastic simple columnar epithelium at gastro-oesophageal junction
(2. ) RF = Caucasians, men, older age, Fx of barretts or oesophageal cancer, GORD, hiatus hernia, obesity, smoking and alcohol intake
(3. ) Presentation = asymptomatic, dysphagia, dyspepsia
(4. ) Ix = Endoscopy and biopsy
(5. ) Mx =
- Lifestyle: Reduce weight, stop smoking, reduce alcohol intake, take smaller meals, avoid hot drinks, alcohol, NSAIDs
- PPI
- Ablative therapy of barratt’s epithelium
- Oesophagectomy if severe dysplasia confirmed
- Screening endoscopy in high risk groups (male, >50, obese, Caucasian, Fx)
(6. ) Complication = oesophageal adenocarcinoma
Gastric Cancer - RF, Sx, Ix, Mx
RF: >55y, men, poor socio-economic status, H.pylori, smoking, Fx
Sx: dyspepsia, weight loss, vomiting, dysphagia, anaemia.
Ix: FBC, endoscopy, biopsy
Mx
- Sx control for pain, nausea, constipation, depression, mouth care
- Surgical resection
- Palliative care
H.Pylori - what bacteria is it? How can it spread? HP Infections (2) ?
- Gram negative and urease positive rod, that colonises gastric epithelium
- Has multiple flagellas that allows it to be very motile and adhere to gastric epithelium
- Acquired via faecal-oral route in children in low socioeconomic and overcrowded areas
Among infected individuals:
- peptic ulcer disease
- inc risk of gastric cancer
What are Peptic Ulcers
Breaks in the mucosal lining of the stomach or duodenum.
Two types of peptic ulcers = duodenal ulcers, gastric ulcers
(6) Causes and RF of peptic ulcers
- Helicobacter infection
- Long term NSAIDs and aspirin
- Zollinger-Ellison Syndrome (gastric tumor causes overproduction of gastric acid)
- Mucosal ischaemia
- Corrosive e.g. chemotherapy, radiation, bile reflux
- Stress
RF = smoking, alcohol, chronic NSAID use, h.pylori infection
Sx of peptic ulcers
(1. ) Bloating
(2. ) Dyspepsia
(3. ) N+V
(4. ) Epigastric pain
(5. ) Early satiety
(6. ) Black tarry stools (melaena) if upper GI bleeding
(7. ) Differentiate between duodenal and gastric ulcers by asking about relationship to food –> in duodenal ulcers it is relieved, in gastric ulcer it worsens.
- Weight loss = gastric
- Weight gain = duodenal
(4) Ix of peptic ulcers
(1. ) Stool and breath test = Detect H.Pylori
(2. ) FBC
(3. ) Endoscopy is dx
(4. ) Imaging
- CXR: test for other causes of epigastric pain.
- CT: evaluate for pancreatitis
*****NOTE: When gastric ulcer is suspected, evaluation for hemodynamic stability is critical as they often present with upper GI bleeding and may have hemorrhagic shock (confusion, low BP, arrhythmias etc)
Treatment and Management of peptic ulcer disease
- PPI
- If h.pylori: eradication therapy = PPI + amoxicillin + clarithromycin
- Surgical Mx if perforation, uncontrolled bleeding present
- Avoid = NSAIDs, tobacco, alcohol, caffeine
Complications of peptic ulcer disease
- Perforation that can lead to peritonitis
2. Haemorrhage
What is Peritonitis
- Inflammation of the visceral and parietal peritoneum
- Onset can be acute of chronic
- Source of origin can be primary or secondary
- Location can be generalised or localised
3 Types of Peritonitis
(1. ) Secondary: if developed after injury or medical condition in abdo cavity
- Aetiology: ruptured appendix, Perforate colon, Stomach ulcer, Abdominal trauma/injury, Crohns disease or diverticulitis, Pancreatitis, Dialysis etc
(2. ) Spontaneous: infection arises from fluid build up (ascites)
- Aetiology: Cirrhosis - spontaneous bacterial peritonitis
(3.) Non-infectious causes: Blood, Gastric juice, Urine, Bile
Causes of Peritonitis
- Bacterial = GI origin (E.Coli, Strep, Ent etc) or Non-GI orgin (Chlamydia, N.Gonorrhoea)
- Chemical - e.g. bile, barium
- Ischaemia from vascular occlusion
- GI perforation peritonitis (perforated ulcer, diverticulum, appendicitis)
- Exogenous contamination E.g. drains, open surgery, trauma, peritoneal dialysis
- Haematogenous spread (rare) E.g. septicaemia
Clinical features of Peritonitis
(1. ) Fever and Chills
(2. ) Abdo pain - localised guarding, shoulder pain
(3. ) N+V
(4. ) Distention
(5. ) Diarrhoea, constipation, minimal U/O
(6. ) Fatigue
rapid deterioration
Investigation of Peritonitis
(1. ) Bloods = high WBC, amylase may suggest pancreatitis etc
(2. ) Imaging = perforated GIT?
(3. ) Peritoneal fluid analysis
(4. ) Urine dipstick = test for UTI
Mx of Peritonitis (6)
(1. ) Correction of fluid loss
(2. ) IV abx
(3. ) Analgesia
(4. ) Consider oxygen
(5. ) Urinary catherization
(6. ) Surgical tx if need to remove infected tissue, repair perforated ulcer, excision of perforated organ.
What are Ascites?
An accumulation of excess serous fluid within the peritoneal cavity. (Healthy men – no fluid, Women up to 20 ml)
Causes of Ascites
Transudates (protein <25 g/L)
• Low plasma protein concentrations syndromes
• High central venous pressure: Congestive cardiac failure
• Portal HTN: Portal vein thrombosis/Cirrhosis (75%)
Exudates (protein >25 g/L)
• Peritoneal malignancy
• Tuberculous peritonitis
• Budd–Chiari syndrome (hepatic vein occlusion or thrombosis)
• Pancreatic ascites
• Others: Chylous ascites , Meigs’ syndrome
Clinical Features of ascites
(1. ) Abdominal distension - Clothes getting tighter
(2. ) Nausea, Loss of appetite
(3. ) Constipation
(4. ) Cachexia- extreme weight loss
(5. ) Associated Sx of underlying cause e.g. Jaundice & Other Stigmata of liver disease
Investigations of ascites
(1.) LFTs, Cardiac function help determine underlying cause
(2. ) Imaging
(a. ) Xray if 500ml
(b. ) US at least 20ml
(c. ) CT if v.small
(3. ) Ascitic aspiration (under imaging guidance)
- Fluid for microscopy, cytology, culture, including mycobacteria, and analysis of protein content and amylase.
Tx and Mx of Ascites
(1. ) Trans-jugular intrahepatic portosystemic shunt (TIPS)
(2. ) Sodium restriction via diet
(3. ) Diuretics
(4. ) Paracentesis - if large volume, up to 4-6L/day with colloid replacement
(5. ) Indwelling drain ( home paracentesis , smaller volumes)
(6. ) Peritoneovenous shunting ( for rapidly accumulating ascites: abandoned)
What is Pancreatitis?
- Pancreatitis occurs when digestive enzymes become activated while still in the pancreas, irritating the cells of your pancreas and causing inflammation.
- Acute is sudden and lasts for days, chronic occurs over years. It is unpredictable where 20% develop life-threatening condition.
Aetiology of pancreatitis
GET SMASHED Gallstones* Ethanol * Trauma Steroids Mumps Autoimmune Scorpion venom Hyperlipidaemia, hypothermia, hypercalcemia ERCP, emboli Drugs
Chronic = alcohol, smoking, autoimmune, familial, pancreatic duction obstruction(stones/tumour), congential
RF of pancreatitis
- Excessive alcohol Consumption
- Smoking
- Obesity
- Fx
Signs and symptoms of acute pancreatitis
Acute
(1. ) Sudden-onset epigastric or LUQ pain, which often radiates to the back
- Sitting forward may relieve it
(2. ) N+V
(3. ) Fever
(4. ) Jaundice
(5. ) Periumbilical (Cullen’s Signs) and flanks bruising (Turner’s Sign)
3 Investigations of pancreatitis
(1. ) Blood: elevated amylase, lipase, CRP
(2. ) Stools: Look at fats, faecal elastase
(3. ) Imaging - if there is a dx doubt
- X-ray
- CT
- US = if gallstones are present
- ERCP/ EUS = visualise pancratic duct dilatation and cysts
- MRCP
Treatment and Management of CHRONIC pancreatitis
Malabsorption Mx
- Lipase, Creon, Fat-soluble vitamins
Other Mx
(1. ) Lifestyle: alcohol, smoking, diet
(2. ) Counselling for alcohol and drug use e.g.CAGE questionnaire
(3. ) Psychiatric conditions e.g. depression
Treatment and Management of ACUTE pancreatitis (5)
If suspected -> ADMIT, do not delay by taking bloods
(1. ) IV fluids
(2. ) Analgesia
(3. ) Nutritional + O2 support
(4. ) Abx if infection, necrosis
(5. ) ERCP if stones
Complications of Pancreatitis (11.)
(1. ) Renal failure
(2. ) Hypocalcemia
(3. ) hyperglycemia, DM
(4. ) Hypovolemia and Tacycardia - SHOCK
(5. ) Breathing Problems - Acute Respiratory Distress Syndrome
(6. ) Disseminated Intravascular Coagulation
(7. ) Pancreatic Necrosis and infection - SEPSIS
(8. ) Pancreatic Pseudocyst
(9. )Malnutrition
(10. ) Pancreatic Cancer
What is assessed using the Glasgow Criteria?
Severity of ACUTE pancreatitis is assessed using Glasgow Criteria - PANCREAS
P - PO2 A – AGE N – NEUTROPHILLS C – CALCIUM R – RENAL FUNCTION E – ENZYMES A – ALBUMIN S – SUGAR
