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Upper GI Flashcards

1
Q

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)

A
  1. Helicobactor pylori which is most commonly detected using a stool antigen test before initiation of treatment.
  2. H2 blockers such as ranitidine and proton pump inhibitors (PPIs) such as omeprazole.
  3. Gastric, duodenal cancer
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2
Q

Barrett’s Oesophagus - pathophysiology, RF, Presentations, Ix,Mx, Complications

A

(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

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3
Q

Gastric Cancer - RF, Sx, Ix, Mx

A

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
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4
Q

H.Pylori - what bacteria is it? How can it spread? HP Infections (2) ?

A
  • 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
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5
Q

What are Peptic Ulcers

A

Breaks in the mucosal lining of the stomach or duodenum.

Two types of peptic ulcers = duodenal ulcers, gastric ulcers

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6
Q

(6) Causes and RF of peptic ulcers

A
  1. Helicobacter infection
  2. Long term NSAIDs and aspirin
  3. Zollinger-Ellison Syndrome (gastric tumor causes overproduction of gastric acid)
  4. Mucosal ischaemia
  5. Corrosive e.g. chemotherapy, radiation, bile reflux
  6. Stress

RF = smoking, alcohol, chronic NSAID use, h.pylori infection

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7
Q

Sx of peptic ulcers

A

(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

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8
Q

(4) Ix of peptic ulcers

A

(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)

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9
Q

Treatment and Management of peptic ulcer disease

A
  1. PPI
  2. If h.pylori: eradication therapy = PPI + amoxicillin + clarithromycin
  3. Surgical Mx if perforation, uncontrolled bleeding present
  4. Avoid = NSAIDs, tobacco, alcohol, caffeine
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10
Q

Complications of peptic ulcer disease

A
  1. Perforation that can lead to peritonitis

2. Haemorrhage

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11
Q

What is Peritonitis

A
  • 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
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12
Q

3 Types of Peritonitis

A

(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

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13
Q

Causes of Peritonitis

A
  1. Bacterial = GI origin (E.Coli, Strep, Ent etc) or Non-GI orgin (Chlamydia, N.Gonorrhoea)
  2. Chemical - e.g. bile, barium
  3. Ischaemia from vascular occlusion
  4. GI perforation peritonitis (perforated ulcer, diverticulum, appendicitis)
  5. Exogenous contamination E.g. drains, open surgery, trauma, peritoneal dialysis
  6. Haematogenous spread (rare) E.g. septicaemia
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14
Q

Clinical features of Peritonitis

A

(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

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15
Q

Investigation of Peritonitis

A

(1. ) Bloods = high WBC, amylase may suggest pancreatitis etc
(2. ) Imaging = perforated GIT?
(3. ) Peritoneal fluid analysis
(4. ) Urine dipstick = test for UTI

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16
Q

Mx of Peritonitis (6)

A

(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.

17
Q

What are Ascites?

A

An accumulation of excess serous fluid within the peritoneal cavity. (Healthy men – no fluid, Women up to 20 ml)

18
Q

Causes of Ascites

A

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

19
Q

Clinical Features of ascites

A

(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

20
Q

Investigations of ascites

A

(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.

21
Q

Tx and Mx of Ascites

A

(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)

22
Q

What is Pancreatitis?

A
  • 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.
23
Q

Aetiology of pancreatitis

A 
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

24
Q

RF of pancreatitis

A
  1. Excessive alcohol Consumption
  2. Smoking
  3. Obesity
  4. Fx
25
Q

Signs and symptoms of acute pancreatitis

A

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)

26
Q

3 Investigations of pancreatitis

A

(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

27
Q

Treatment and Management of CHRONIC pancreatitis

A

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

28
Q

Treatment and Management of ACUTE pancreatitis (5)

A

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

29
Q

Complications of Pancreatitis (11.)

A

(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

30
Q

What is assessed using the Glasgow Criteria?

A

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

GI (12 decks)

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