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Surgery - 3rd year > Dyspepsia > Flashcards

Dyspepsia Flashcards

1
Q

What is dyspepsia?

A

“a range of upper gastrointestinal (GI) symptoms lasting 4 weeks or more including heartburn, indigestion, upper abdominal pain or discomfort, gastric reflux, nausea or vomiting”

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2
Q

Dyspepsia - DDx

A
  • GORD
  • H pylori gastritis
  • gastric or duodenal ulcer (PUD)
  • barrett’s oesophagus
  • hiatus hernia
  • oesophageal cancer
  • functional dyspepsia
  • coeliac’s
  • autoimmune gastritis

Consider gallstones, pancreatitis, IBS, cardiac causes

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3
Q

GORD - definition

A

Reflux of stomach contents causing troubling symptoms that affect wellbeing or that cause complications.

Symptoms or complications resulting from the reflux of gastric contents into the oesophagus or beyond, into the oral cavity (including larynx) or lung.

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4
Q

GORD - clinical features (common)

A

RF = family history of heartburn or GORD; obesity; older age; or hiatus hernia.
- heartburn = burning sensation in the chest after meals
can be worse after lying down or bending over. Can occur at night but is not usually exertional.
- Reflux = acid reflux into the mouth, with a sour or bitter taste, mainly after meals.

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5
Q

GORD - clinical features (uncommon)

A

dysphagia
bloating/early satiety
laryngitis
globus (lump in throat present despite swallowing)
enamel erosion (teeth erosion)
halitosis
some meds can exacerbate = NSAIDs, CCBs, bisphosphonates, theophylline, steroids

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6
Q

GORD - investigations

A
  • Clinical Dx
  • therapeutic trial of PPI can serve for both diagnosis and initial treatment
  • Upper endoscopy is indicated to evaluate for complications; for atypical, persistent, or relapsing symptoms; or for alarm features (e.g., weight loss, anaemia)

hiatus hernia –> barium swallow
barrett’s –> OGD

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7
Q

GORD - lifestyle changes

A 
	Weight loss
	Dietary fat reduction
	Smoking cessation
	Reduce alcohol
	No food 3 hours before bed 
	Frequent, moderate amount meal 
	Elevate bed-head
	Avoidance of caffeine or spicy foods
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8
Q

GORD - treatment

A
  • OTC alginate+antacid = gaviscon
  • Offer empirical full dose PPI therapy for 4-8 weeks – (BNF) Omeprazole 20mg PO once daily for 4-8 weeks
  • If symptoms return then use PPI/H2A at lowest dose to control symptoms – add Ranitidine for 8-12 weeks
  • Refractory/complicated: consider surgery: fundoplication, GOJ and hiatus are dissected and the fundus wrapped around the GOJ, recreating a physiological LOS
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9
Q

PPI - common interaction and S/E

A

Omeprazole (P450 inhibitor) reduces the effect of clopidogrel by decreasing its activation by P450 enzymes (normally P450 inhibitors would cause an increase in the effect of other drugs)

Common S/E of PPIs = abdominal pain, constipation, diarrhea, flatulence, headache, N+V

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10
Q

What are red flags for oesophageal cancer 2WW referral?

A

Offer urgent direct access upper GI endoscopy (to be performed within 2 weeks) to assess for oesophageal (and gastric) cancer in people:

  • With dysphagia OR
  • Aged 55 and over with weight loss and any of:
    Upper abdominal pain
    Reflux
    Dyspepsia
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11
Q

What is H pylori?

A

A curved, gram-negative, rod-shaped (bacilli) bacterium

Associated with peptic ulcer disease
60-70% of gastric ulcers (GU)
90% of duodenal ulcers (DU)

Transmission is via the oral-faecal route
or possibly oral-oral

May be protective against oesophageal cancer

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12
Q

What does H pylori infection increase risk of?

A
  • gastritis
  • peptic ulcer disease
  • Gastric adenocarcinoma

H. pylori infection –> chronic active gastritis –> atrophic gastritis –> intestinal metaplasia –> dysplasia –> gastric adenocarcinoma

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13
Q

What tests can be done to detect H pylori?

A
  • urea breath test = pts swallow urea labelled with an isotope eg carbon-14. Detection of isotope-labelled carbon dioxide in exhaled breath indicates that the urea was split and that urease is present in the stomach
  • H pylori faecal antigen test
  • H pylori rapid urease test = on biopsy tissue obtained during endoscopy. The tissue is placed in an agar gel containing urea, a buffer, and a pH-sensitive indicator. In the presence of H pylori urease, the urea is metabolised to ammonia and bicarbonate and detected as a colour change.
  • gastric mucosal histology
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14
Q

Peptic Ulcer Disease (PUD) - definition

A

A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter, with depth to the submucosa. Ulcers smaller than this or without obvious depth are called erosions. Peptic ulcers result from an imbalance between factors promoting mucosal damage (gastric acid, pepsin, H pylori, NSAID use) and mechanisms promoting gastroduodenal defense (prostaglandins, mucus, bicarbonate, mucosal blood flow).

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15
Q

PUD - clinical features (general)

A
  • RF = H pylori, NSAIDs, aspirin, smoking, increasing age, previous or family history
  • abdominal pain centred in upper abdomen
  • may have epigastric tenderness

Less common:

  • nausea relieved by eating, and vomiting can occur after eating. May indicate pyloric stenosis
  • may have anorexia
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16
Q

Gastric ulcers - features

A
  • Middle aged/older aged population
  • Pain worse while eating or about 30 min after
  • Gastro-toxic medications often implicated (Aspirin/NSAIDs/Steroids) & smoking
  • H.Pylori implicated in >60%
  • Malignancy must be considered 1-2%
17
Q

Duodenal ulcers - features

A
  • Younger and usually male
  • Food relieves the pain initially / pain 2-5 hours after eating
  • Nocturnal pain more common
  • H.Pylori implicated in >90%
  • Malignancy is very rare
  • pain may be severe and radiate through to back as a result of penetration of the ulcer into the pancreas
18
Q

PUD - investigations

A

Helicobacter pylori urea breath test or stool antigen test
upper gastrointestinal endoscopy
FBC (check anaemia)

19
Q

PUD - treatment

A
  • stop NSAID/aspirin
  • H pylori -ve = PPI 1st line, H2A 2nd line
  • H pylori +ve = PPI + clarythromycin + amoxicillin or metronidazole (triple therapy) (AND metronidazole = quadruple therapy) for about 2 weeks
  • active bleeding ulcer = fluids or transfusion + OGD with sclerotherapy or can inject adrenaline. If not settled, laparotomy and under running of the ulcer
  • perforation: suturing +/- vagectomy to reduce relapse rate; For chronic gastric ulcer: anthrectomy
20
Q

PUD - complications

A

Immediate:
- Upper GI bleeding: ulcer erodes into the wall of a gastroduodenal blood vessel. NSAIDs are the major risk factor for peptic ulcer bleeding
- Perforation: Caused by erosion of the ulcer through the wall of the stomach or duodenum. Usual presentation is with shock and peritonitis.
(AXR –> pneumoperitoneum)
Long Term:
- Penetration: chronic ulcer penetrates the entire thickness of the stomach or duodenal wall
- Gastric outlet obstruction: may present with nausea, vomiting, and weight loss

21
Q

GORD - complications

A
  • oesophageal ulcer, haemorrhage, or perforation
  • oesophageal stricture
  • Barrett’s oesophagus
  • adenocarcinoma of the oesophagus
22
Q

Barrett’s Oesophagus - definition

A

Change in the normal squamous epithelium of the oesophagus to specialised intestinal metaplasia. This is associated with gastro-oesophageal reflux, even if the reflux is asymptomatic. Essential to the diagnosis is histology demonstrating columnar-lined epithelium, with or without intestinal metaplasia and with goblet cells

the main concern is the increased risk of adenocarcinoma of the oesophagus

23
Q

Oesophageal adenocarcinoma - risk factors

A
  • male sex
  • tobacco use
  • excessive alcohol intake
  • GORD and Barrett’s oesophagus
  • family history of oesophageal, stomach, oral, or pharyngeal cancer
  • low socioeconomic status
  • diet low in fresh fruit and vegetables

NOT H pylori
(could actually be a protective factor)

24
Q

Oesophageal adenocarcinoma - features

A
  • dysphagia
  • odynophagia
    Possible signs
  • hoarseness (recurrent laryngeal involvement)
  • hiccups (phrenic nerve involvement)
  • postprandial/paroxysmal cough (oesophagotracheal or oesophagobronchial fistula)
  • enlarged virchow’s node (left supraclavicular)
    (also enlarged in gastric, breast, lung cancer, lymphoma)
  • Dx: Upper GI endoscopy + CT chest, abdo, pelvis
  • Tx: surgical resection (Ivor- Lewis type oesophagectomy) with intrathoracic oesophagogastric anastomosis
    +/- neoadjuvant chemotherapy prior to surgery
  • Cx: anastomotic leak with mediastinitis
25
Q

Barrett’s Oesophagus - treatment

A
  • non dysplastic: endoscopic surveillance, high dose PPI +/- radiofrequency ablation
  • low grade dysplasia: radiofrequency ablation with or without endoscopic mucosal resection
  • high grade dysplasia: 1st line –> as per low grade + PPI. 2nd line –> oesophagectomy

Surgery - 3rd year (10 decks)

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