Unit 5 Ch 33, 34: GI System and Peptic Ulcer Disease

Chief cells

secrete pepsinogen, inactive form of pepsin which chemically breaks down proteins

Parietal cells

secrete HCl and intrinsic factor

Hydrochloric acid

produced by parietal cells in stomach; breaks down food, activates pepsinogen, kills ingested microbes

Intrinsic factor

produced by parietal cells in stomach; essential for vitamin B12 absorption

Enterendocrine cells

secrete hormones that coordinate digestive processes, ex. gastrin, stimulates HCl production by parietal cells

Duodenum

first part of the small intestine, where chyme mixes with bile from gallbladder and digestive enzymes from pancreas

Jejunum

second part of the small intestine, primary site of nutrient and drug absorption

Ileum

third part of the small intestine, primary site of absorption of B12, long-chain fatty acids, fat-soluble vitamins

Colon/large intestine

reabsorbs water and electrolytes from waste material, excretes fecal matter, contains host flora (synthesizes vitamin K and B-complex vitamins)

Accessory organs of digestion

teeth, tongue, salivary glands, liver, gallbladder, pancreas

Liver functions

regulation, protection, synthesis, storage

Liver regulatory function

stabilizes the serum levels of glucose, triglycerides, and cholesterol

Liver protective function

removes toxic substances and waste products such as ammonia

Liver synthesis function

synthesizes bile, plasma proteins, certain clotting factors

Liver storage function

stores iron and fat-soluble vitamins

Cytochrome P450

enzyme system in liver that metabolizes drugs

Hepatic portal system

veins that collect blood from digestive system and deliver to liver before reaching arterial circulation

Enterohepatic recirculation

drugs or metabolites that are excreted in bile, reabsorbed from the small intestine, returned to the liver, metabolized, and eventually excreted in urine

Enteric nervous system

network of neurons in the submucosa or the alimentary canal that has sensory and motor functions

- chemoreceptors, stretch receptors

Peptic ulcer

a lesion located in either the stomach (gastric) or the small intestine (duodenal)

Peptic ulcer disease risk factors

- H. pylori infection

- NSAIDs, ASA, glucocorticoids

- family hx

- blood group O

- tobacco, caffeine

- stress

NSAID promotion of ulcer formation

- direct cellular damage to GI mucosal cells

- interferes with prostaglandin synthesis via COX in stomach

- decreases gastric blood flow, slows cellular repair

- weak acids that are nonionized in gastric acid, diffuse into gastric epithelial cells

Cyclooxygenase (COX) enzyme

converts arachidonic acid into prostaglandins and aids in the production of mucus and bicarbonate

Zollinger-Ellison syndrome (ZES)

less common cause of PUD, caused by a gastrinoma

Gastrinoma

pancreas tumour or duodenum that secretes large amounts of gastrin; can lead to ZES

Gastrin

hormone that stimulates the secretion of HCl in the stomach; too much HCl > ulcers

Crohn's disease

ulceration in the distal small intestine

Ulcerative colitis

erosions in the large intestine

Inflammatory bowel disease

Crohn's disease + ulcerative colitis

Duodenal ulcer symptoms

gnawing or burning upper abdominal pain that occurs 1 to 3 hrs after a meal

- deeper erosion: bleeding, hematemesis, melena

Gastric ulcer symptoms

pain relieved by food, anorexia, weight loss, vomiting

Gastroesophageal reflux disease (GERD)

acidic stomach contents entering the esophagus; caused by relaxation/weakening of the lower esophageal sphincter

GERD symptoms

heartburn, dysphagia, dyspepsia, chest pain, nausea, belching; worse after large meals, exercise, or reclining

Barrett's esophagus

condition associated with increased risk for esophageal cancer; can be a complication of GERD

Pharmacotherapy of PUD and GERD

- H2-receptor antagonists

- proton pump inhibitors

- antacids

- antibiotics

- misc drugs

H2 receptor

histamine receptor, increase acid secretion in stomach

H2-receptor antagonists

suppress the volume and acidity of stomach acid; ex. cimetidine, ranitidine

Cimetidine

H2 receptor antagonist; used less frequently than others because of drug-drug interactions (inhibits hepatic drug-metabolizing enzymes)

Nursing implications - H2-receptor antagonists

- assess for kidney and liver function; smaller dose with diminished kidney function

- may lead to vit. B12 deficiency bc decreased absorption

- may need iron supplements bc best absorbed in acid

- monitor CBC

- monitor use of OTCs

Symptoms of H2-receptor antagonists

dizziness, drowsiness, confusion, headache

Ranitidine

prototype H2-receptor antagonist; blocks H2 receptors in the stomach to decrease acid production

- more potent than cimetidine, fewer drug-drug interactions

Proton pump inhibitors

act by binding to and blocking the enzyme H+, K+-ATPase and reduce gastric acid secretion

- more effective at reducing acid longer duration of action than H2-receptor antagonists

- ex. omeprazole

H+, K+-ATPase

enzyme responsible for pumping acid (H+ ions) onto the mucosal surface of the stomach from

Nursing implications - proton pump inhibitors

- monitor liver function

- monitor serum gastrin; oversecretion occurs with constant acid suppression

- 30 mins before eating; unstable in acidic environment and enteric coated

- can be same time as antacids

- sleep with head elevated

- eat food with beneficial bacteria

Proton pump inhibitors for H. pylori

usually administered in combination with clarithromycin

Omeprazole

prototype PPI; reduces acid secretion by binding to H+, K+-ATPase

- also treats ZOS

Antacids

alkaline substances (inorganic aluminum, Mg2+, Na+, Ca2+) that neutralize stomach acid; OTC

Simethicone

sometimes added to antacids bc it reduces gas bubbles that cause bloating and discomfort

Sodium antacids

should not be taken by clients on sodium-restricted diets, or those with HTN, HF, or renal impairment; may promote fluid retension

Magnesium antacids

can cause hypermagnesemia (fatigue, hypotension, dysrhythmias), and also acts as a laxative in the large intestine

Calcium antacids

can cause constipation, kidney stones, hypercalcemia, or renal failure, or milk-alkali syndrome

Milk-alkali syndrome

caused by administering calcium carbonate antacids with milk or vit. D; can result in permanent renal damage

- headache, urinary frequency, anorexia, nausea, fatigue

Aluminum antacids

can cause constipation, but balanced with Mg2+ salts

___ carbonate or hydroxide may interfere with phosphate absorption > hypophosphatemia

Bicarbonate antacids

may cause metabolic alkalosis, or bloating and belching (combines with gastric acid to form CO2)

Antacid interaction with weak acid drugs

the pH of the stomach rises (more basic) > less ionized drug > less readily absorbed, less therapeutic effect

Antacid interaction with weak base drugs

pH of the stomach rises (more basic) > more ionized drug > more readily absorbed, more therapeutic effect

Antacid interaction with enteric-coated or delayed-release drugs

stomach pH rises (more basic) > "fools" the tablets into dissolving early and releasing contents into stomach > irritates stomach lining, causes nausea + vomiting, or is inactivated

Antacid interaction with antibiotics

may bind and form complexes with them, preventing them from being absorbed; ex. tetracyclines, digoxin

Antacid interaction with urine pH

makes the pH more basic > increases the excretion of acidic drugs (ex. ASA) and inhibits the excretion of basic drugs (ex. amphetamines)

Nursing implications - antacids

- assess for renal insufficiency; caution with Mg2+-containing antacids

- Mg2+ and aluminum-based = diarrhea

- Ca2+-based = constipation

- HF or HTN, avoid Na+-based

- 2 hrs before or after oral meds

- white stools

Antibiotics for H. pylori

- amoxicillin

- clarithromycin

- metronidazole

- tetracycline

- bismuth subsalicylate (Pepto-Bismol)

Antibiotic combinations for H. pylori

- 2+ concurrently to increase effectiveness and lower risk of resistance

- PPI or H2-receptor antagonist

- bismuth compounds

Bismuth compounds

inhibit bacterial growth and prevent H. pylori from adhering to gastric mucosa; Pepto-Bismol

Misc drugs for PUD

- sucralfate

- misoprostol

- metoclopramide

Sucralfate

consists of sucrose (sugar) + aluminum hydroxide (antacid); produces a gel-like substance that coats the ulcer, protecting it against further erosion and promoting healing

- does not affect gastric acid secretion, little absorbed from GI tract

- constipation

Misoprostol

prostaglandin-like, inhibits gastric acid secretion and stimulates production of protective mucus; prevents peptic ulcers with NSAIDs + glucocorticoids

- diarrhea, abdominal cramping; contraindicated in pregnant clients

Metoclopramide

short-term therapy of GERD or PUD when first-line agents fail; treats nausea + vomiting from surgery or chemo

- causes muscles in the upper intestine to contract = faster stomach emptying

- decreases esophageal relaxation

- CNS effects; drowsiness, fatigue, confusion, insomnia