Clinical Pharmacy

Department

Clinical Pharmacy And

Drug Information
PL 504
Lecture 7
Interactive Teaching

• OSCE
• Audio-visual learning
• Case studies
 References

• ACCP Updates in Therapeutics® 2020:

Pharmacotherapy Preparatory Review and
Recertification Course

• Walker, Roger, and Cate Whittlesea. Clinical

Pharmacy and Therapeutics. Edinburgh:
Churchill Livingstone, 2007.
 Lecture LOS
By the End of the lecture student will be able to

 Identify different types of PUD and the appropriate

management

 Recognize and manage of GERD

 Recognize and manage of Inflammatory bowel disease

 Peptic Ulcer
• An ulcer is defined as a breach in the gastric or duodenal mucosa
down to the submucosa.
Classification of peptic ulcer disease (PUD)
Duodenal ulcer Gastric ulcer
Presentation
• Epigastric pain, possibly • Epigastric pain, often
worse at night. Often, pain made worse by eating
occurs 1–3 hours after a
meal and may be relieved
by eating.

• Associated symptoms can • Associated symptoms may

include heartburn, include heartburn,
belching, a bloated belching, a bloated
feeling, nausea, and feeling, nausea, and
anorexia anorexia
 Causes
• The two main causes of peptic ulcer disease are
H. pylori infection and the use of aspirin and
NSAIDs.

• Some NSAIDs such as

• ibuprofen, diclofenac, and nabumetone
are intrinsically less toxic to the GI tract
than
• Naproxen, which is considered a
moderate risk.
• Other agents such as piroxicam,
indomethacin, and ketorolac are
considered high-risk agents.
Risk factors
 N.B: Stress ulcer
Stress ulcers are ulcers that form due severe physiological stress, such as
head injury, spinal cord injury, burns, multiple trauma or sepsis.
Complications of PUD

a. Bleeding
b. Gastric outlet obstruction( tissue
inflammation and edema result in
mechanical obstruction.)
c. Perforation
 Diagnosis of peptic ulcer
A-Clinical manifestations
B- Investigations:
Endoscopy Radiology H. pylori detection

Double-contrast barium A- Noninvasive tests

radiography detects - Serological test
80% of peptic ulcers but - Urea breath test
is only done where (UBT)
endoscopy has failed or - Stool antigen test
the patient declines B- Invasive tests
endoscopy. (endoscopic tests)
 Endoscopy
• Endoscopy is generally the investigation of choice for diagnosing the underlying cause
of dyspepsia, although the investigation is invasive and expensive.
• Routine endoscopy in patients presenting with dyspepsia without ALARM features is
not necessary but should be undertaken in patients with ALARM features and in those
patients older than 55 years who present with unexplained or persistent symptoms of
dyspepsia.
Endoscopy

ALARM
features
H. pylori detection tests
1- Non invasive UBT and Stool antigen test
Patients should discontinue anti-secretory agents(e.g. H2 blocker, PPI)
or antibiotics at least 2 weeks before UBT and stool antigen testing or
wait 4 weeks after treatment of H pylori has ended before having the
UBT or stool antigen test performed.

2- Invasive (Rapid urease tests)

Patients should discontinue anti-secretory agents for at least 1 week
before the test is performed
 Primary prevention
• A- Test and treat for H. pylori infection if the
patient is beginning long-term NSAID therapy.

• B- Determine the level of GI-related risk (low,

medium, high) for strategies to prevent GI
complications in patients receiving NSAIDs
based on their CV risk.
Risk Factors category for NSAID-Induced
Gastrointestinal Complications

Ketorlac >40 mg/day

Primary prevention of NSAID-induced ulcers
N.B:
• The AHA recommends that ibuprofen be taken at least
30 minutes after or 8 hours before the ingestion of
immediate-release low-dose aspirin to prevent the
ibuprofen from attenuating the antiplatelet effects of
the aspirin.

• One study of naproxen and low-dose aspirin has

suggested naproxen may interfere with aspirin’s anti-
platelet activity when they are co-administered.
However, naproxen 500 mg administered two hours
before or after the administration of aspirin 100 mg did
not interfere with aspirin’s antiplatelet effect. There is
no data looking at doses of naproxen less than 500mg
 Treatment
Documented
peptic ulcer

H pylori positive H pylori negative H pylori Positive H pylori negative

(negative NSAID ) (positive NSAID) NSAIDS positive (NSAID negative

H pylori PPI 8 PPI 8 weeks

eradication PPI 4-8
weeks + eradication weeks
therapy therapy
 Initial treatment
• Offer H. pylori eradication therapy to people who
have tested positive for H. pylori and who have peptic
ulcer disease.
 H. pylori eradication

• Eradication speeds healing of ulcers and reduces recurrence.

• The standard regimen is a triple therapy consisting of:

a PPI, clarithromycin and amoxicillin or metronidazole in a twice-daily

simultaneous course
 H. pylori eradication

• The other core choice for first-line therapy, especially in regions with high
primary clarithromycin resistance, is bismuth-based quadruple therapy.

• It involves a PPI, bismuth, tetracycline, and metronidazole (PPI-BTM).

 Initial treatment
Offer full-dose PPI or H2RA therapy
for 8 weeks if on NSAIDs and stop
the use of NSAIDs where possible

And

4 to 8 weeks to people who have

tested negative for H. pylori who
are not taking NSAIDs
 Initial treatment
• if H. pylori is present With NSAIDS , subsequently
offer eradication therapy
 Anti-secretory therapy

Proton pump inhibitors:

 Anti-secretory therapy

Proton pump inhibitors:

• Drug interactions:
Omeprazole and esomeprazole are potent inhibitors of CYP450, and therefore they
may increase the levels of drugs that are metabolized by this isoenzyme (e.g.
warfarin)
Absorption of the antifungals; ketoconazole and itraconazole is reduced by
omeprazole due to a reduction in acidity required for absorption. This is likely to be a
class effect of PPIs, and concomitant use should be avoided.
 Anti-secretory therapy

H2-receptor antagonists:
• The role of H2-receptor antagonists in the management of dyspepsia has
diminished because PPIs are more effective and generally recommended
as first line.
 Anti-secretory therapy

H2-receptor antagonists:(Cimetidine, ranitidine, famotidine, nizatidine)

• S.E: Diarrhea and headache are the most common, and occasionally
mental confusion and rashes have been reported. Hepatotoxicity is a
rare adverse effect.
• Cimetidine, due to its antiandrogenic effects, has been associated with
gynecomastia and impotence when used in high doses.
 Anti-secretory therapy
H2-receptor antagonists:
Drug interactions:
• Cimetidine is an inhibitor of a number of the cytochrome P450
isoenzymes and therefore inhibits the metabolism of many drugs, which
is potentially important for drugs with a narrow therapeutic index.
• Cimetidine is now rarely used in practice.
• The H 2 blocker ranitidine (Zantac) has been withdrawn from the
U.S. market because of concerns over levels of the contaminant
N-nitrosodimethylamine, which can increase with time and
temperature, posing a risk of cancer. Patients should be told to
discard all products containing ranitidine.
 Case 1
A 68-year-old woman, Ms WR, presents for review of her medication. Her medical history includes hypertension and
osteoarthritis of the knees. Ms WR receives a regular prescription for the following:
• bendroflumethiazide 2.5 mg daily, • naproxen 500 mg twice daily.
Ms WR stopped smoking 4 years ago. She is overweight, with a body mass index (BMI) of 30 kg/m2. Her blood pressure is
148/92 mmHg with a pulse of 82 beats/min.
The results of Ms WR’s routine blood tests are as follows: Value Reference range
Sodium 138 mmol/L 135–145 mmol/L
Potassium 3.9 mmol/L 3.4–5.0 mmol/L
Creatinine 110 mmol/L 75–155 mmol/L
Blood glucose 6.8 mmol/L <11.1 mmol/L
Total cholesterol 4.5 mmol/L <4.0 mmol/L
Haemoglobin 12.0 g/dL 11.5–16.5 g/dL
• Questions
2. What is the risk associated with NSAID use in this patient?
3. What are the options for minimizing the risk of peptic ulceration?
Case 2
• A 23 years old male visited clinic with complains of an upper abdominal pain,
heartburn, nausea and sometimes vomiting. He was in usual state of health 5
days back when he started having epigastric pain. Pain aggravated at night
after taking large meal. He was fond of fried and spicy food. He had a family
history of peptic ulcer disease. He denied cigarette smoking.
• General examination
• Weight: 58kg
• Height: 5feet 8inches
• BMI: 19.44kg/m2
• Temperature: 98°F
• BP: 120/70mmHg
• Hemoglobin:13.5
• Questions
• What are the required investigations at this stage?
• If this patient approved to be +ve H.pylori infection, explain the suitable initial
treatment.
Gastro-oesophageal reflux disease
 Gastro-oesophageal reflux disease

 Treatment duration of at least 4 weeks with PPI if no erosive esophagitis

present; erosive esophagitis should be treated with an 8-wk course of PPIs; no
major differences between PPIs

 Use maintenance PPIs if return of symptoms or complications

 Long-term maintenance should be the lowest effective dose, on demand, or

intermittent therapy

 Bedtime H RAs can be used if morning PPI and nighttime symptoms, but
2

tachyphylaxis develops

 Further testing needed before use of metoclopramide (prokinetic) or baclofen

(skeletal muscle relaxant)
 1. Proton pump inhibitors (Omeprazole, Pantoprazole):

i. “Step-down” treatment: starting with maximal therapy, such as therapeutic

doses of PPIs, is always appropriate as a first-line strategy in patients with
documented esophageal erosion.

Advantages: rapid symptom relief, avoidance of over-investigation.

Disadvantages: potential overtreatment, higher cost, increased potential for

adverse effects.
 1. Proton pump inhibitors (Omeprazole, Pantoprazole):

ii. “Step-up” treatment: starting with lower-dose over-the-counter (OTC)

products for patients with less severe symptoms without evidence of
esophageal erosion.

Advantages: avoids overtreatment, has lower initial cost.

Disadvantages: potential under-treatment (partial symptom relief; may take

longer for symptom control; may lead to over-investigation).
 Non – pharmacological
• A- Dietary modifications if symptoms are associated with
certain foods or drinks. Routine global elimination of food
triggers is not recommended

i. Avoid aggravating foods and beverages; some may reduce LES pressure
(e.g., alcohol, caffeine, chocolate, citrus juices, garlic, onions, peppermint,
spearmint) or cause direct irritation (e.g., spicy foods, tomato juice, coffee).

• ii. Reduce fat intake (high-fat meals slow gastric emptying) and portion size.

• iii. Avoid eating 2–3 hours before bedtime.

• iv. Remain upright for 2 hours after meals.

 Non – pharmacological

• B- Weight loss if overweight (body mass index greater than 25

kg/m2) or recent weight gain

• C- Reduce or discontinue nicotine use in patients who use

tobacco products (affects LES)

• D- Elevate head of bed if nocturnal symptoms present

• E- Avoid tight-fitting clothing (decreases intra-abdominal

pressure).
 Case studies
Mr LP, aged 64 years, is attending a medication review clinic. While discussing any
concerns Mr LP has about his medication, he mentions that he suffers from heartburn.
On further questioning, Mr LP explains that his heartburn has been recently getting
worse, and that food occasionally “gets stuck” when he is eating. Mr LP has a past
medical history of hypertension, angina and heart failure. He lives alone and smokes
30–40 cigarettes per day, he has no medical insurance.
Mr LP’s medication history is as follows:
• aspirin 75 mg daily,
• ramipril 5 mg twice a day,
• furosemide 40 mg each morning,
• metoprolol 200 mg each morning,
• isosorbide mononitrate MR 30 mg each morning,
• simvastatin 40 mg at night,
• GTN spray 1–2 sprays when required.
1. What is the non-medication advice can you offer to Mr LP?
2. Endoscopy showed no erosive esophagitis. What recommendations could
you make regarding Mr LP’s drug therapy?
 Inflammatory Bowel Disease
(IBD)
Inflammatory bowel diseases are a group of inflammatory
conditions in which the body’s own immune system attacks parts of
the digestive system.
 Crohn’s Disease Ulcerative Colitis
Can affect any part of the GI tract (from the Occurs in the large intestine (colon) and the
mouth to the anus)—Most often it affects the rectum
portion of the small intestine before the large
intestine/colon.

Damaged areas appear in patches that are Damaged areas are continuous (not patchy) –
next to areas of healthy tissue usually starting at the rectum and spreading
further into the colon
Inflammation may reach through the multiple Inflammation is present only in the innermost
layers of the walls of the GI tract layer of the lining of the colon
 IBD managemnt

• Aminosalicylates, such as sulfasalazine, mesalamine,

olsalazine and balsalazide, are medicines containing 5-
aminosalycylic acid, an aspirin-like compound. They reduce
inflammation in the lining of the intestine and are used in
mild to moderate cases.
• Corticosteroids, including budesonide, prednisone and
prednisolone, are steroids that are used as short term
treatment during flares. They act on the immune system and
suppress its ability to begin and maintain inflammation.
 IBD managemnt

• Immunomodulators, such as azathioprine, cyclosporine and

methotrexate, affect the body’s immune system so that it is
unable to maintain an inflammatory response. Unlike
steroids, however, they are a long-term treatment.
• Biologic therapies, including infliximab, adalimumab,
certolizumab pegol, golimumab, lizumab and natalizumab,
are antibodies grown in the laboratory that stop certain
proteins in the body from causing inflammation.
 IBD
vs
Irritable Bowel Syndrome (IBS)

• Irritable bowel syndrome is not a disease, but rather a

condition that affects the function and behavior of the
intestines.
 Faculty of
Pharmacy