GI Medications

Peptic ulcer disease

Peptic ulcer disease

Refers to a group of upper GI disorders characterized by varying degrees of erosion of the gut wall.

Most common in lesser curvature of the stomach and duodenum

Where does peptic ulcer disease occur?

After a meal when the stomach is empty (2-3 hours later)

When do people with PUD typically experience abdominal discomfort?

1. Weight loss

2. poor appetite

3. bloating

4. belching

5. nausea

6. vomiting

Signs and symptoms of peptic ulcer disease: [6]

Melena

When blood mixes with feces. Stool is black and almost tarry. Comes from GI bleed.

Right away. GI bleeding is a medical emergency.

When should GI bleeds be checked?

1. blood in vomit

2. Vomit with coffee grounds consistency

3. Blood in stool

4. black stool

Signs of a GI bleed: [4]

1. Mucous

2. Bicarbonate

3. Blood flow

4. Prostaglandins

Defensive mechanisms for PUD (prevents the stomach lining from acid)

1. H. Pylori

2. NSAIDS

3. Gastric acid

4. pepsin

5. Smoking

Aggressive factors for PUD (causes/.makes it worse)

1. Hydrogen binds to receptors in parietal cells in the stomach

2. This stimlates cAMP production

3. cAMP increases kinase activation

4. kinase increases activity of enzyme H+-K+ATPase

5. Increases hydrogen pumped into the duodenum

6. Stomach acidity increases

How does a normal proton pump work? [6]

When there is an imbalance between mucosal defensive factors and aggressive factors

When do peptic ulcers occur?

Bicarbonate

Secreted by epithelial cells of the stomach and duodenum. Most is trapped in the mucus layer, where it neutralizes any hydrogen ions that penetrate the mucus.

Sufficient blood flow is essential for maintaining mucosal integrity. If blood flow is reduced, local ischemia can lead to cell injury, making it more likely to attack by acid and pepsin.

Why is blood flow an important defensive factor against peptic ulcers?

These compounds stimulate secretion of mucus and bicarbonate and promote vasodilation. They also suppress the secretion of gastric acid.

How do prostaglandins help defend from peptic ulcers?

H. Pylori

BActeria that can colonize the stomac and duodenum, living in the space between epithelial cells and the mucus barrier that protects these cells. Believed cause of PUD.

NSAIDS inhibit prostaglandins.

How do NSAIDS cause ulcers?

Breath test or serum

How to test for H. Pylori: [2]

1. alleviate symptoms

2. promote healing

3. prevent complications (ex: anemia)

4. prevent recurrences

Treatment goals for PUD [4]

1. Antibiotics

2. Anti-secretory agents

3. Mucosal protectants

4. Antacids

Classes of drugs that treat ulcers: [4]

1. Amoxicillin

2. Clarithromycin

Antibiotics used to treat H. Pylori causing PUD [2]

H2RAs

Ex: Famotidine (Pepcid)ss

Anti-secretory drugs that decreases volume of acid in the stomach (name example)

Suppresses acid secretion by

1. Blocks hydrogen receptors on parietal cell wall

2. Inhibits enzyme that generates acid (H+-K+ATPase)

MOA for H2RAs:

can be taken oral or IV, and the same rate with or without food.

How are H2RAs absorbed?

Their distribution is limited, so there are few side-effects

How are H2RAs distributed?

Long-term treatment, low doses (20mg bid po)

H2RA treatment:

MOA for omeprazole

Omeprazole (Prilosec/losec)

Proton pump inhibitor:

They inhibit gastric secretion. They irrevesible inhibition of the enzyme that generates gastric acid, so dose is only given once a day for 4-8 weeks.

What do proton pump inhibitors do?

1 hour

NOTE: although half life is short, this drug has irreversible action on enzymes, therefore lasts 3-5 days.

Half-life of proton pump inhibitors

1. They bind to enzyme that generates acid

2. Causes irreversible inhibition for the life of that enzyme

3. decrease hydrogen in stomach/duodenum lumen

4. Decrease aggressive factors

MOA of proton-pump inhibitors

1. Headache

2. N&V&D

3. Increased risk of pneumonia

4. Rebound acid secretion if stop abruptly

Omeprazole adverse effects:

Not well known, but can increase osteoporosis. May be carcinogen.

Omeprazole long term adverse effects:

1. antacid binds with hydrogen

2. Neutralizes it in the stomach

3. Decreases irritation of the mucosa by hydrogen

4. increases stomach pH

   1. Decreased pepsin activation

   2. Decreased irritation by pepsin

Antacid MOA:

They act locally on the stomach and do not alter systemic pH(ex: blood pH)

Why is it good that antacids have poor absorption?

Relief of gastric reflux

Therapeutic use of antacids:

Would need to be on a regular schedule and not just PRN (7xday). This is why they are normally just for symptomatic relief.

Dose required for antacids to promote some healing and not just alleviate pain:

1. Constipatio (alumnum hydroxide)

2. Diarrhea (magnesium hydroxide)

3. Sodium loading

Adverse effects of antacids:

It can increase or decrease the excretion of some drugs. Drugs prefer a pH where they become ionzed. If a drug cannot be excreted, this can lead to toxicity.

Why is it an issue when antacids alkalize urine (less acidic)?

1. Warfarin

2. Digoxin

3. Tetracycline

Antacids bind and decrease the drug availability of which drugs? [3]

Misoprostol (Cytotec)

Prostaglandin analogues (replaces prostaglandins):

Patients on long term NSAIDs (NSAIDs inhibit prostaglandins)

When might a patient be prescribed misoprostol?

1. Replaces pGE2 (prostaglandin enzyme) in the gut

2. Acts like prostaglandin to:

   1. Suppress gastric secretions

   2. Increase HCO3 and cytoprotective mucous

   3. Increase vasodilation to maintain blood flow

Misoprostol (cytotec) MOA:

It can stimulate uterine contractions

Why isn’t misoprostol (cytotec) given to pregnant patients?

1. Dose related diarrhea

2. Abdominal pain

Adverse affects of prostaglandin analogues: [2]

Usually 200mcg po 4 times per day

MIsoprostol (cytotec) dosing:

1. Added in acidic conditions

2. Polymerizaion and cross-linking reactions occur

3. Becomes a viscous/sticky gel that adheres to the ulcer crater

4. Barrier back diffusion of H+, pepsin and bile salts.

Sucralfate/Carafate MOA:

Stool

How are cytoprotective agents excreted?

Acute and maintenance treatment of gastric and duodenal ulcers. Protectice barrier up to 6 hours, available in tablets and suspension.

Therapeutic use of cytoprotective agents (Sulcralfate/carafate):

1gm 4 times per day, before meals and at bedtime for 4-6 weeks

Cytoprotective agent (sulcralfate/carafate) dosing:

Antacids raise pH and decrease effectiveness

How do antacids affect cytoprotective agents?

1. Phenytoin

2. Digoxin

3. Warfarin

4. fluoroquinolones

Cytoprotective agents should be given 2 hours apart from which dugs because it may interfere with their absorption?

1. Vitamins

2. Iron-rich foods (if blood loss)

3. Bland diet

4. Avoid coffee and alcohol

5. Fat, calcium, and coffee oils Stimulate acid

6. Smaller, more frequent meals

Changes in diet for ulcer treatment [6]

Constipation

Difficult, incomplete, or infrequent evacuation of dry, hardened stool. Determined by altered consistency rather th

LAxatives

Used to ease or stimulate defecation.

1. soften stool

2. increase stool volume

3. hasten fecal passage

4. fascilitate evacuation from the rectum

Laxatives will: [4]

1. True diagnosis f constipation

2. Hemorroids and bleeding from straining

3. To prevent impaction with bedridden/paralyzed patients

4. Constipation from pregnancy or drugs

5. Straining that increases myocardial demand (valsalva maneuver)

6. loss of abdominal and perineal muscle tone in the elderly

Indications for mild laxative use: [6]

Cathartic laxatives

Laxatives that cleanse the bowel

1. Obtaining a stool sample

2. cleansing the bowel pre-op

3. Emptying bowel prior to x-rays

4. Removal of poisons

Indications for cathartic laxative use:

Acute surgical abdomen

When the bowel is touched (ex: in surgery) and it temporarily stops moving

1. Abdominal pain/cramps/nausea (could be appendicitis etc.)

2. acute surgical abdomen

3. Fecal impaction/obstruction

4. habitual use (dependent)

Contraindications of laxatives:

RIsk perforating the bowel

Why wound’t laxatives be given for impaction/obstruction?

1. Bulk-forming

2. Surfactant

3. Stimulant

4. Osmotic

5. Miscellanious

Classifications of laxatives: [5]

bulk-forming laxatives: Psyllium (Metamucil)

Laxatives that are natural or semi-synthetic polysaccharides and celluloses from plants. Increases bulk of stool.

1. swells in water and becomes a viscous gel

2. Softens fecal mass and increases bulk

3. Stretches intestinal wall to stimulate peristalsis

Bulk-forming laxative (metamucil/psyllium) MOA

1. For temporary relief

2. preventiive

3. diverticulitis

4. irritable bowel syndrome

5. elderly

When are bulk-forming laxatives given? [4]

250mL of water

Bulk-forming laxatives should be taken with what?

1-3 days

Onset of bulk-forming laxatives

1. Lowers surface tension of stool so water blends with stool

2. inhibits fluid absorption by intestinal wall

3. Stimulates secretion of water and electrolytes into intestine

Surfactant laxatives MOA

Docusate sodium (Colace)

Surfactant laxatives:

1. Increases water and elctrolytes held in the intestine for softer feces

2. Stimulates intestinal motility

Stimulant laxatives MOA:

Bisacodyl (dulcolax)

Stimulant/contact laxatives

PO: 6-12 hours

Rectal: 15-60 minutes

Stimulant laxative onset:

castor oil

Used as a cathartic laxative because its a potent stimulant laxative

milk irritant, can cause cramping

Stimulant laxative potential side effects:

Osmotic laxatives (magnesium hydroxide, Milk of Magnesia)

Laxatives that draw water from the lumen, causing fecal mass to swell

1. Made from poorly absorbed salts

2. Draws water from intestinal lumen by osmotic action

3. Water causes fecal mass to swell

4. Swell stretches the intestine and stimulates peristalsis

Osmotic laxatives MOA

1. dehydration

2. Toxic if magnesium and potassium accumulate (if have kidney problems)

3. Contraindicated for heart failure and HTN due to fluid retention

osmotic laxatives adverse effects: [3]

1. mineral oil

2. Lactulose

3. glycerin suppository

Miscellaneous laxatives: [3]

indigestible oils allow lubcrication. By enema, used for fecal impaction.

Adverse: systemic intake, fat deposits on liver

Mineral oil as laxative MOA:

mulk forming from mild osmotic action. sed for those who don’t respond to bulk-forming laxatives

LActulose as laxative:

osmotic agent that softens and lubricates. 30 minute onset, often used in children

Glycerin suppository MOA

1. increase activity and movemnt

2. increase fluid/fibre intake

3. heed the urge

4. Allow time and don’t rush

non drug methods for treatng/preventing constipation [4]

Diarrhea

Excessive volume, fluidity and frequency of bowel movements

1. infection

2. poor digestion

3. inflammation

4. mediation side effect (antibiotics)

5. Substances (lactose, gluten)

6. Disorders (IBS, Chrohn’s, ulcerative colitis)

Causes of diarrhea

1. Diagnose and treat underlying disorde

2. replacement of fluid and electrolytes

3. relief of cramping

4. reducing unformed stool

Goals of diarrhea management:

1. Hydration status

2. serum electrolytes

3. hepatic and renal function before meds

4. Any contraindications

If patient has diarrhea, what should the nurse consider assessing?

1. pregnancy and lactation (can cross placenta/breast milk

2. severe dehydration

3. electrolyte imbalance

4. liver/renal disorders (metabolism/excretion)

5. Glaucoma (some meds increase IOP)

6. Down’s syndrome (shorter bowels)

Contraindications/caution for antidiarrheals

1. Changes to salicylate in the GI tract

2. Inhibits prostaglandins responsible for Gi hypermotility and inflammation

Bismuth subsalicylate (Pepto-Bismol) MOA

Aspirin is the same chemical compound (a salicylate).

Why shouldn’t people who are sentivite to aspirin take pepto bismol?

Increases the effectiveness of oral anti hyperglycemics and blood sugars can go low

Why shouldn’t diabetics take pepto bismol?

Pepto bismol can increase the amount of uric acid in blood

Why shouldnt patients with gout take pepto bismol?

diphenoxylate (lotomil)

Opioid for diarrhea:

Diphenoxylate (lotomil)

Oral medication with morphine-like effects only with high doses. Controlled diarrhea drug.

Loperamide (imodium)

Opioid-like drug that suppresses fluid secretion into the intestinal lumen. No opioid effect.

Decreases motility

decreases secretions of fluid into small intestine

Increases absorption of fluid and salt

Active opioid for diarrhea MOA

don’t treat unless severe. BOdy is trying to get rid of the bug. Usually after a few days

When to treat infectious diarrhea:

Bulks up stool, gives it a firmer consistency.

Why might bulk-forming agents be given for diarrhea?

Directly stimulates the vomiting center that receives signals from the brain, senses, or inner ear.

Indiret stimulation activates the chemo-receptor trigger zone 1st (signals from the stomach and other drugs)

Where do antiemetics act?

Ondansetron (zofran)

Seratonin receptor antagonist. “golden nugget” normally given with chemo drugs that cause lots of nausea. Given orally or IV

Blocks type 3 seratonin recpetors in afferent vagal nerve in chemoreceptor trigger zone

Ondansetron (Zofran) MOA