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Pharmacy > 301 Dyspepsia, GORD & peptic ulcers > Flashcards

301 Dyspepsia, GORD & peptic ulcers Flashcards

1
Q

What is gastro-oesophageal reflux (GOR)?

A

Condition affecting GI tract whereby the acidic contents of stomach are able to flow back into oesophagus

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2
Q

What is heartburn?

A

When stomach acid comes in contact with oesophagus lining, patient may experience burning sensation in chest or throat

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3
Q

What is the difference between GOR and GORD?

A

When symptoms become more frequent & affect person’s wellbeing
Symptoms occur two or more times a week

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4
Q

What is dyspepsia?

A

Pain or discomfort (including upper abdominal pain, heartburn, reflex, bloating/fullness, early satiety, bloating or nausea) centred in upper abdomen/GI tract
Symptoms >4 weeks

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5
Q

Oesophagus anatomy

A

Muscular tube about 25cm long
Tube collapsed when not involved in transporting food to stomach
Takes fairly straight course throughout thorax
Goes through oesophageal hiatus to enter abdomen

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6
Q

What is the lower oesophageal sphincter (LOS)?

A

Where oesophagus joins stomach, there is thickening of circular smooth muscle
Extends 3cm above juncture with stomach

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7
Q

How do LOS and diaphragm act together?

A

Acts as a valve to keep stomach contents out of oesophagus
Diaphragm muscle helps to ensure integrity of seal

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8
Q

What does LOS do whilst swallowing?

A

Receptive relaxation of LOS allows passage of food from oesophagus into stomach

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9
Q

Difference between LOS and oesophagus in terms or pressure

A

LOS normally constricted (pressure of 15-30mmHg) - oesophagus mid-point is relaxed

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10
Q

Why is the pressure of LOS important?

A

The tonic constriction of LOS prevents significant reflux of highly acidic contents of stomach into oesophagus

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11
Q

Why might presence of acidic stomach contents in oesophagus be an issue?

A

Reflux oesophagitis occurs in patients with GERD when toxic substances such as gastric acid, pepsin & bile salts come into contact with the oesophageal mucosa, resulting in damage to the distal oesophageal mucosa

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12
Q

What happens in GORD?

A

Reflux occurs when there is loss of LOS tone
Relaxation of sphincter naturally occur as vagal reflex when stomach distends
Allows small amount of acid into oesophagus after meals
Called transient lower oesophageal sphincter relaxations (TLOSRs)

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13
Q

GORD patients and TLOSRs

A

In GORD patients TLOSRs are more likely to be associated with acid reflux

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14
Q

When are gastric contents more likely to reflux?

A

Gastric volume increased
After meals, if gastric emptying is impaired, obstructions
Gastric contents are near junction
Posture (bending down, reclining)
Gastric pressure is increased
Obesity, ascites (fluid build-up in abdomen), pregnancy, tight clothes

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15
Q

Causes of GORD

A

Genetic - family history
Age - increased age
Gender - male or pregnancy
Dietary triggers - spicy, fatty, chocolate, mint, caffeine
Obesity - overweight, increased risk of hiatus hernia
Stress
Medication
Smoking

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16
Q

Which medications cause GORD?

A

NSAIDs (indomethacin vs ibuprofen)
Calcium channel blockers (nifedipine)
Nitrates
Antibiotics (doxycycline)
Bisphosphonates (alendronate) - sit up 30 mins after taking
Iron supplements (pregnancy)
Quinine
Potassium supplements
Anticholinergics
TCAs
Progesterone
BZDs
Theophylline

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17
Q

What is hiatus hernia?

A

Structural abnormality in which superior part of stomach protrudes slightly above diaphragm through diaphragmatic hiatus
Most often due to abnormal relaxation or weakening of sphincter

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18
Q

How does the diaphragm aid in maintaining anti-reflex barrier?

A

Retention of gastric contents and acid above diaphragm can result in increased volumes of gastric juice entering oesophagus

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19
Q

What is hiatus hernia caused by and risk factors?

A

Caused by sharp, physical exertions which increase abdominal pressure (coughing, vomiting, straining)
Obesity and pregnancy can increase risk, as can increasing age
80% of hiatus hernias are sliding

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20
Q

Why do symptoms occur in GORD?

A

Oesophageal epithelium is not able to handle gastric juices for extended periods of time
Level of damage depends on frequency of episodes & volume of gastric juice entering oesophagus

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21
Q

Patient experiences in GORD

A

Heartburn - feeling of burning rising up from stomach or lower chest towards neck
Regurgitation
Waterbrash - acidification of oesophagus causes sudden stimulation of salivation - mouth fills with saliva

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22
Q

Atypical symptoms of GORD

A

Chest pain (caution)
Cough
Asthma
Throat/voice changes

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23
Q

GORD complications: reflux oesophagitis

A

Complication of reflux where mucosal defences are unable to counteract damage caused by acid, pepsin and bile

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24
Q

GORD complications:
non erosive oesophagitis

A

Mucosa may be normal or mildly erythematous (redness due to dilated capillaries)

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25
Q

GORD complications: erosive oesophagitis

A

Clear mucosal damage with redness, friability (solid substance breaking into smaller pieces when stressed/rubbed) & ulcers, persistent damage can lead to stricture formation

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26
Q

GORD complications: Barrett’s oesophagus

A

Complication of long-standing reflux, distal squamous epithelium converted to columnar epithelium, increases relative risk of patient developing adenocarcinoma of oesophagus 30-125 fold, although lifetime risk still low (<2%)

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27
Q

GORD complications: Strictures
Adenocarcinoma of oesophagus

A

Abnormal narrowing of the oesophageal lumen
Type of oesophageal cancer that develops in the glandular cells of the oesophagus

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28
Q

GORD in babies

A

Common (~40% of infants)
Does not usually require investigation
If distressed behaviour, gagging, choking, faltering growth, chronic cough, single case of pneumonia then medical treatment needed

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29
Q

GORD in babies: breast-fed

A

Feeding assessment then add in alginate trial (1-2 weeks Gaviscon Infant Sachets maximum 6 in 24 hours)

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30
Q

GORD in babies: bottle-fed

A

More frequent smaller feeds, thickened formula such as Carobel, Enfamil AR

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31
Q

What can dyspepsia be caused by?

A

Can be caused by reflux or peptic ulcer disease (PUD)
Can be mild and self-limiting

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32
Q

Dyspepsia: alarm signs or RED flags

A

GI bleeding
Difficulty swallowing
Weight loss
Abdominal swelling
Vomiting
If >50-55 years with new onset - refer
<18 years - refer
Any alarm signs present - advise to see GP urgently

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33
Q

Endoscopy - what percentage have these disorders:
Functional dyspepsia (“non-ulcer”)
Oesophagitis
Peptic (GU/DU) ulcers
Barrett’s oesophagus
Gastric cancer

A
  1. 60%
  2. 20%
  3. 13%
  4. 1.4%
  5. 3%
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34
Q

Aims of dyspepsia treatment

A

Manage symptoms
Treat underlying causes of dyspepsia
Do not exacerbate co-morbidities

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35
Q

Dyspepsia lifestyle changes

A

Healthy eating, weight reduction and smoking cessation
Avoid fatty foods, spicy foods and onions, citrus fruits and juices, tomatoes
Obesity, smoking, coffee and chocolate can cause reduction in LOS
Fatty foods may delay gastric emptying
Raising bed head at night may also reduce acid regurgitation
Avoid eating large meals before bed
Consider withdrawal of precipitant medications

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36
Q

Dyspepsia: pharmacological measures

A

Antacids
- Neutralised HCl secreted by gastric parietal cells
- Can be used for dyspepsia, PUD, GORD
- Liquid preparations more effective but less convenient
E.g. aluminium hydroxide, calcium carbonate, magnesium salts

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37
Q

Why do we need to take care with these antacids?
Aluminium hydroxide
Calcium carbonate
Magnesium salts

A

Constipation - aluminium and calcium
Diarrhoea - magnesium salts
Avoid antacids with high Na content - heart failure, renal failure, cirrhosis (chronic liver disease) & oedema
Avoid aluminium in renal disease as this may accumulate

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38
Q

DIs with antacids

A

Phenytoin - can reduce absorption of phenytoin and cause loss of seizure control
Quinolones - reduced absorption causing loss of antibiotic efficacy
Antacids with alginates - rafting agents increases viscosity of stomach contents and protects oesophageal mucosa from acid contents
Antacids with simethicone - antifoaming agents to relieve flatulence (can be used to relieve hiccoughs (hiccups) in palliative care)

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39
Q

What should be done with DIs and antacids?

A

Antacids should not be taken at same time as other drugs
Take antacid 2 hours before or after other meds

40
Q

Dyspepsia: H2 receptor antagonists

A

E.g. cimetidine, famotidine, nizatidine, ranitidine
Competitively block H2 receptors on parietal cell Reducing gastric acid secretion
Adverse effects: usually well tolerated, side effects reported in 1-2% cases

41
Q

Dyspepsia: cimetidine and side effects

A

Slurred speech, confusion states (elderly), interacts with androgen receptors occasionally causing gynaecomastia & galactorrhoea, thrombocytopenia, granulocytopenia, neutropenia, reversible cholestatic jaundice with cimetidine

42
Q

Dyspepsia: ranitidine side effect

A

Reversible hepatitis

43
Q

DIs with H2 receptor antagonists

A

Phenytoin, carbamazepine - reduces anticonvulsant clearance causing possible toxic effects
Theophylline - reduced theophylline clearance causing possible toxic effects
Avoid effervescent tabs in Na+ restriction - heart failure, renal impairment

44
Q

Why are ranitidine and cimetidine no longer in use?

A

Ranitidine withdrawn from UK market due to link to NDMA, a probable human carcinogen increase over time
Cimetidine also linked and no longer used due to side effects

45
Q

Dyspepsia: proton pump inhibitors

A

E.g. Esomeprazole, Lansoprazole, Omeprazole, Pantoprazole, Rabeprazole
Irreversibly inactivate hydrogen/potassium ATPase enzyme system thus suppressing both stimulated & basal acid secretion

46
Q

Dyspepsia: proton pump inhibitors side effects

A

Generally well tolerated, occasional headache, tiredness, rarely - antiandrogenic effects, deranged LFTs, thrombocytopenia

47
Q

Dyspepsia: other treatment agents

A

Sucralfate - adsorbs pepsin and decreases its concentration
Misoprostol - inhibits basal and nocturnal gastric acid secretion through direct stimulation of prostaglandin E1 receptors on parietal cells in the stomach

48
Q

Dyspepsia: initial management
Uninvestigated dyspepsia
Functional dyspepsia

A
  1. PPI for 4 weeks
    Test for H.Pylori and if positive, treat
    (If high risk for H.Pylori, test first or in parallel with PPI)
  2. Test for H.Pylori and if positive treat
    If H.Pylori negative - PPI or H2 antagonist for 4 weeks
49
Q

Dyspepsia: follow up treatment
1. Patients with refractory symptoms
2. If symptoms persist or recur after initial treatment
3. If uninvestigated dyspepsia taking NSAID (but NSAID can’t be stopped)
4. If uninvestigated dyspepsia taking aspirin (but aspirin can’t be stopped

A
  1. Assess for new alarm symptoms and consider alternative diagnoses
    Check adherence to original management and lifestyle measures
  2. PPI or H2 antagonist at lowest dose to control symptoms (PRN therapy may be considered)
  3. Consider reducing NSAID dose or (if possible) switch to paracetamol or COX-2-inhibitor, consider using long-term gastro-protection with acid suppression therapy
  4. Consider switching aspirin to alternative antiplatelet agent
50
Q

Dyspepsia: general follow up management points

A

Patients given H.Pylori eradication so not need regular testing
Patients with dyspepsia should receive annual review of symptoms and treatment
(A “stepped down” approach should be encouraged)
Refer to specialist if patient has unexplained/unresponsive GO symptoms or if H.Pylori does not respond to 2nd line therapy

51
Q
A
52
Q

What is peptic ulcer disease (PUD)?

A

Disruption of mucosal integrity of stomach and/or duodenum leading to local defect or excavation due to active inflammation

53
Q

What does PUD represent?

A

An imbalance between protective factors that normally maintain mucosal integrity and destructive factors (gastric acid, pepsin etc.)

54
Q

What are ulcers?

A

Breaks in mucosal surface >5mm in size that reach sub-mucosa
They form when there is an imbalance between protective and destructive factors present in stomach and duodenum

55
Q

3 protective measures of gastro-duodenal defence mechanisms

A

Mucous/bicarbonate layer
Surface epithelial cells
Prostaglandins

56
Q

Gastro-duodenal defence mechanisms: mucous/bicarbonate layer

A

Produced by epithelial cells
Contains water & lipids and glycoproteins (mucin)
Layer impedes diffusion of ions & molecules - sets up pH gradient, pH 1-2 at luminal surface and 6-7 on epithelial surface

57
Q

Gastro-duodenal defence mechanisms:
Surface epithelial cells

A

Cells not only produce mucus
Have tight junctions forming protective seal
Cells can be replaced quickly and undergo constant turnover

58
Q

Gastro-duodenal defence mechanisms:
Prostaglandins

A

Gastric mucosa contains high levels of prostaglandins
Regulate mucosal bicarbonate and mucous release, inhibit parietal cell secretion & maintain blood flow and epithelial cell repair/replacement

59
Q

PUD epidemiology:
Gastric ulcers (GU)
Duodenal ulcers (DU)

A
  1. Occur more frequently later in life (60s)
    Less common than DU
    Often silent (no symptoms)
    Diagnosed when complications occur
  2. Occur in 5-15% western population
    Mortality & morbidity associated with disease has decreased >50% in last 30 years, may be due to H.Pylori eradication
60
Q

PUD - pathology
DU
GU

A
  1. Located within 3cm of pylorus in 90% cases, rarely malignant
  2. Can represent malignancy
61
Q

PUD - causes:
DU
GU

A
  1. H.Pylori & NSAID induced injury account for majority
    Appears to be increase in average basal & nocturnal acid secretion in patients with DU
    Bicarbonate secretion appears to be decreased
  2. H.Pylori and NSAID also implicated in majority of cases
    Increased acid reflux, delayed gastric emptying
62
Q

PUD: Symptoms

A

Epigastric pain described as burning or gnawing can be present in both DU & GU
Discomfort also described as ill-defined aching or hunger pain
Typical pain pattern in DU is 90 mins to 3 hrs after meal, frequently relieved by antacids or food
Pain worsened by food
Nausea & weight loss also more common in GU

63
Q

PUD: Causative factors

A
  1. NSAIDs (aspirin, ibuprofen, diclofenac)
    Anything can interrupt prostaglandin synthesis can cause ulcer formation
  2. Other factors
    Mental stress
    Smoking
    Corticosteroids
    Zollinger-Ellison syndrome (presence of gastric-secreting tumour)
    Blood group O
64
Q

What do prostaglandins maintain?

A

Gastro-duodenal integrity

65
Q

What is Zollinger-Ellison syndrome?

A

Rare syndrome
Cells in pancreas release gastrin
Leads to high gastric acid production & severe ulcer disease
Extrapancreatic gastrinomas which release gastrin can occur (usually wall of duodenum) and surgery is indicated
Requires much higher doses of PPIs long term

66
Q

Complications of PUD

A

Gastric outlet obstruction & intestinal perforation & haemorrhage (potentially life-threatening)

67
Q

PUD: Patients at high risk of complication with NSAID are…

A

Those with history of complicated PU OR
TWO or more of the following
- >65 years of age
- High dose NSAIDs
- Other meds with increased risk of PU (SSRIs, anticholinergic, steroids)
- Serious co-morbidities (CVD, HTN, diabetes, renal or hepatic disease)
- Heavy smoker
- Excess alcohol intake
- Previous ADR to NSAIDs
- Prolonged need for NSAIDs

68
Q

PUD: diagnosis

A

Endoscopy - invasive - direct exam of oesophagus, stomach & duodenum
H.Pylori can be diagnosed using urea breath test - non-invasive (other methods faecal antigen test, laboratory-based serology & biopsy-based methods)

69
Q

What are the gold-standard tests for PUD diagnosis?

A

Stool antigen test or 13C urea breath test or endoscopy with biopsy, serology tests only if locally validated

70
Q

What should patients do with medication before their endoscopy?

A

Patients free from meds with PPI for min. 2 weeks beforehand
H2 antagonist use is fine, no anti-bacterials 2 weeks before test

71
Q

PUD: treatment aims

A

Promote ulcer healing
Manage symptoms
Treat H.Pylori infection if detected
Reduce risk of ulcer complications & recurrence
Not exacerbate co-morbidities

72
Q

PUD: non-pharmacological management

A

Healthy eating, weight loss, avoid food triggers, eat smaller meals, eat evening meal 3-4 hours before bedtime & rise bedhead, smoking reduction and then cessation, avoid alcohol (reduction initially), avoid ulcerogenic drugs, avoid caffeine (gastric acid stimulant), stress/anxiety/depression management

73
Q

When is an urgent endoscopy needed in suspected PUD?

A

If dysphagia present OR significant GI bleeding OR in those aged 55 yrs OR unexplained weight loss, upper abdominal pain, reflux or dyspepsia

74
Q

PUD: Steps of initial management

A
  1. Stop meds and recreational drugs can induce ulcers if possible: NSAIDs, steroids, SSRIs, KCl, crack cocaine
  2. Antacids used short term but long-term not recommended
  3. Test for H.Pylori
75
Q

PUD: pharmacological management, test results of H.Pylori
If positive without Hx of NSAIDs
Ulcer associated with NSAIDs
H.Pylori negative without Hx of NSAIDs

A
  1. H.Pylori eradication
  2. PPI for 8 weeks - followed by H.Pylori eradication if H.Pylori positive
  3. PPI or H2 antagonist for 4-8 weeks
76
Q

PUD: follow up management, dependent on lesion size

A

Patient with PU who test positive for H.Pylori should:
- Be reviewed 6-8 weeks after eradication treatment and re-tested
- Repeat endoscopy to confirm healing after 6-8 weeks
If ulcer healed and NSAIDs still required - review NSAIDs every 6 months, consider PRN use, reduced dose, switching to paracetamol or alternative analgesic

77
Q

What is acid suppression therapy?

A

Co-prescribed for gastro-protection, PPI preferred (alternatives - H2 antagonist or Misoprostol)

78
Q

PUD: What happens if symptoms recur after initial treatment?

A

PPI may be used at lowest dose to control symptoms on “as needed” basis

79
Q

PUD: What happens if symptoms persist or unhealed ulcer?

A

Check adherence, check other causes (Ca, H.Pylori, meds), switch to alternative acid suppression therapy

80
Q

PUD: H.Pylori eradication regimens

A

Triple therapy for 1 week: high dose PPI, clarithromycin and either amoxicillin or metronidazole
Consider previous exposure to clarithromycin or metronidazole due to high resistance rates

81
Q

PUD: H.Pylori eradication regimens
What if ulcer is large or complicated or perforated?

A

Continue PPI for at least another 3 weeks

82
Q

1st line treatment of PUD (triple therapy)
Acid suppressant
Antibacterial
2nd antibacterial

A
  1. Lansoprazole 30mg BD or Omeprazole 20-40mg BD
  2. Amoxicillin 1g BD or if allergic to penicillin clarithromycin 500mg BD
  3. Either clarithromycin 500mg BD or metronidazole 400mg BD, if allergic to penicillin use metronidazole option
83
Q

PUD: 2nd line treatment
Acid suppressant
Antibacterial
2nd antibacterial

A
  1. Same as first line with either clarithromycin or metronidazole (whichever was not used 1st line)
    If allergic to penicillin and no previous exposure to quinolone
  2. Lansoprazole 30mg BD or Omeprazole 20-40mg BD
  3. Metronidazole 400mg BD
  4. Levofloxacin 250mg BD
84
Q

What should be prescribed with NSAIDs (including coxibs)?

A

PPIs for anyone with osteoarthritis or rheumatoid arthritis
Anyone 45 years + with chronic low back pain
High risk of GI side effects (65+ or using them long term)
History of GI bleed, dual antiplatelet therapy, concomitant oral anticoagulation/antiplatelet/NSAID
(Use the cheapest PPI)

85
Q

NSAID usage and PUD risk:
If NSAID is clinically necessary

A

Consider low-dose ibuprofen (1200mg/day or less) or naproxen (1000mg/day or less) as 1st line

86
Q

What do warfarin and NOACs increase risk of?

A

Bleeds not ulceration

87
Q

What PPI should be used as cover with other medications in PUD (are they taking antiplatelets, SSRIs, corticosteroids, nicorandil?)

A

Consider lansoprazole 15mg (no difference with 30mg)
Co-prescribing omeprazole/esomeprazole with clopidogrel should be avoided

88
Q

What are ulcer-inducing drug examples?

A

Antiplatelets, NSAIDs, anticoagulants, SSRIs, iron-containing therapies, corticosteroids

89
Q

When is PPI usage licensed?

A
  1. Short-term treatment of PUD (gastric and duodenal)
  2. Eradication of H.Pylori (in combo with antibiotics)
  3. Prevention & treatment of NSAID-associated ulcers
  4. Gastro-protection in patients with Hx of dyspepsia & taking aspirin post CVA, MI
  5. Long-term in Barrett’s and Zollinger-Ellison syndrome
  6. Treating dyspepsia
90
Q

Who is at higher risk of clostridium difficile infection?

A

Frequent PPIs more than doubled patient risk
Elderly & broad spectrum antibiotics

91
Q
A
91
Q

What does achlorhydria (stomach does not produce enough HCl) result in?

A

Malabsorption of calcium & vitamin B12

92
Q

What is a rare complication and increased risk of PPI use?

A
  1. Interstitial nephritis
    Severe cases of hypomagnesaemia rarely reported
  2. Pneumonia
    Dementia
93
Q

PPI use: RAHS-rebound acid hypersecretion syndrome, how to avoid?

A

Try alternate day dosing before stopping

94
Q

What is rare SCLE (subacute cutaneous lupus erythematosus)?

A

Non-scarring dermatosis can develop in sun-exposed areas

Pharmacy (23 decks)

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