GI Drugs

Function of the GI Tract

◦ Food digestion
◦ Absorption of nutrients and water

Primary GI disorders:

◦ 1) Damage 20 to gastric acid secretion
◦ Drugs: Manage acid production
◦ 2) Abnormal food movement through the GI tract (gastric motility)
◦ Excessive motility (diarrhea)
◦ Reduced motility (constipation)
◦ Management of emesis (N & V)

Cephalic phase

◦ Anticipation of food (sight, smell) initiates release of stomach acid
◦ Parietal cells secrete acid (for pH between 1-4)
◦ Mucoid cells secrete mucus for stomach lining protection

Gastric phase

◦ Gastrin released when antrum stretched
◦ Triggers release of more gastric acid

Intestinal phase

◦ Chyme enters duodenum
◦ Triggers negative feedback for reducing gastric acid/proteolytic enzyme action in stomach
◦ Release of bicarbonate solution and pancreatic enzymes to aid in digestion

gastric acids (HCl)

• essential for activating digestive protease activity and controlling intestinal bacteria BUT can cause severe ulceration of the stomach lining with accompanying hemorrhage if produce in excessive amounts or the stomach lining is damaged

Acid-reducing agents work by stopping this process (ulceration)

◦ Proton pump blocked by histamine blockers, anticholinergic agents, and proton pump inhibitors (PPIs)
◦ Prostaglandins E2 and I2 (PGE2 and PGI2) also inhibit proton pump

Peptic Ulcer Disease (PUD)

◦ Ulcerations of the mucosal lining of the esophagus, stomach and/or duodenum

GERD

◦ Stomach contents leak backwards from the stomach into the esophagus
◦ AKA: Heartburn or acid indigestion

antiacids MOA

neutralize gastric activity

antacid use

treat acid reflux; increases stomach pH from 1.3 to 3.5 which produces symptomatic relief and some ulcer healing

antacid AE

effervescent types (i.e., Alka-Seltzer) have high sodium content
◦ Drug-drug interaction: increased pH causes reduced absorption of acidic drugs and increased absorption of basic drugs
◦ Avoid taking within 2 hours of other oral medication

H2 receptor antagonist MOA (-tidine)

reduce secretion of stimulated acid

H2 receptor antagonist use (-tidine)

treat acid reflux and heal ulcers

H2 receptor antagonist AE (-tidine)

Best taken HS, usually well-tolerated
AE: diarrhea, muscle pain, rashes

proton pump inhibitor (-prazole) MOA

irreversibly inhibits H+/K+ - ATPase pump on parietal cell membrane which blocks final step in acid secretion into lumen of stomach

proton pump inhibitor (-prazole) use

treat acid reflux and heal ulcers (shown to be more effective than H2 receptor antagonists)

proton pump inhibitor (-prazole) AE

generally well-tolerated; long-term use associated with gastric polyps, altered calcium metabolism (decreased bone mineralization), some cardiovascular abnormalities

Bismuth chelate

Appears to coat ulcer, enhance prostaglandin synthesis, increase gastric mucous epithelial cell growth to protect against H. pylori-induced ulcers.

Sucralfate

An aluminum salt of sucrose that forms a protective coating over the ulcer; used for high-risk cases (trauma, burns, ARDS, major surgery, etc)

Misoprostol

Synthetic prostaglandin analog (PGE2) that inhibits acid secretion; used to prevent NSAID-induced ulcers

what can H. pylori Infection cause?

chronic gastritis, PUD, GERD, gastric cancer

H pylori combo therapy

acid controlling drug + antibiotic

• eliminating bacterium essential to prevent recurrence of ulcer

• can eliminate within one week

NSAID induced ulcer

need to treat H.pylori infection plus add acid suppression therapy
◦ Discontinue use of NSAIDs if possible
◦ Use PPI (misoprostol) or GI-friendly COX-2 inhibitor (but with cardiac risks)

patient positioning: acid related

individuals with GERD should avoid lying flat (supine)
◦ Avoid increased intra-abdominal pressure
◦ Avoid exercise immediately after meals

what is vomit with bright red blood a sign of?

peptic ulcers

Chemoreceptor trigger zone (CTZ)

◦ Floor of 4th ventricle in cerebrum
◦ Responds to toxins/drugs in blood, CSF

Anticholinergics MOA

binds to ACh receptors on vestibular nuclei, blocks communication

anticholinergics AE

dizziness, drowsiness, dry mouth, blurred vision, dilated pupils, difficulty with urination

what drug is used to prevent motion-sickness related vomiting

anticholinergics, antihistamines

antihistamines MOA

inhibit vestibular input to the CTZ

antihistamine AE

dizziness and sedation

Neuroleptic drugs MOA & prokinetic drugs MOA

block dopamine receptors in CTZ

neuroleptic drugs AE

OH, tachycardia, blurred vision, dry eyes, urinary retention, long-term use can lead to extrapyramidal symptoms, akinesia, tardive dyskinesia

prokinetic drugs AE

sedation, diarrhea, weakness, prolactin release; prolonged use causes extrapyramidal signs, motor restlessness. Other possible AE: hypo- and hypertension, tachycardia

what drug produces central and peripheral antiemetic effects?

prokinetic drugs

Serotonin blockers MOA

block serotonin receptors in GI tract, CTZ, and vomiting center

serotonin blockers AE

HA, dizziness, diarrhea, [no extrapyramidal signs]
◦ *Corticosteroids may be used in combination to control chemo-induced emesis

what drug prevents vomiting (emesis

serotonin blockers

Neurokinin-1 receptor blockers MOA

blocks Substance P from binding to NK-1 receptor, prevents both central and peripheral stimulation of vomiting centers

Neurokinin-1 receptor blockers AE

sedation, GI issues (diarrhea, constipation, gas, stomach pain, nausea), ... Stevens-Johnson syndrome

what drug is newer and prevents emesis from chemo?

neurokini 1 receptor blockers

Cannabinoids use

block acute and delayed emesis, used for chemo-induced nausea/vomiting

Cannabinoids AE

ataxia, light-headedness, blurred vision, dry mouth, weakness, tachycardia or bradycardia, CNS symptoms (confusion, anxiety, mood changes)

Phosphorated carbohydrate solution (Emetrol) MOA

relaxes GI tract smooth muscle

Phosphorated carbohydrate solution (Emetrol) use

reduces nausea by working directly on walls of GI tract
◦ Used for mild cases of intestinal flu or food-borne causes

concerns with N/V

A “relative hold” for physical therapy
◦ Reason for N/V?
◦ Consider other factors, such as vitals, body temp, etc.
◦ Ensure pt given anti-emetic medication prior to physical
therapy
◦ Weigh cost-benefit of proceeding with PT
Very common post-op
◦ Same-day discharge for joint replacement and orthopedic surgeries
Give patient an emesis bag and keep extras on hand
Use empathy during communication with the patient
◦ Let patient make final decision to participate in PT

Absorbents MOA

binds to bacteria causing diarrhea to carry them out with feces

Absorbents AE

aspirin product: use with caution in children recovering from flu/chickenpox, increased bleeding time, GI bleed, tinnitus
◦ *Decrease effectiveness of many drugs (digoxin, hypoglycemic drugs, anticoagulants)

Anticholinergics- diarrhea

reduce peristalsis of GI tract
◦ Examples: atropine, hyoscyamine
◦ Because of AE, rarely first choice for treatment

Intestinal flora modifiers

bacterial products obtained from Lactobacillus organisms
◦ Normally resides in intestines to keep “bad” bacteria in check
◦ “gut microbiota”
◦ Helps restore normal balance to suppress harmful organisms

Opiates

decrease GI motility and propulsion
◦ Slowing transit time in intestines = absorption of water and electrolytes
◦ Can also reduce pain
◦ Lomotil has added atropine to prevent recreational opioid use
◦ AE: sedation, dizziness, constipation, nausea, vomiting, respiratory depression, bradycardia, hypotension, urinary retention

diarrhea concerns

May be a “relative” hold for physical therapy
◦ Why does the patient have diarrhea: acute vs chronic disease condition
◦ Consider other factors: N/V, body temp, etc
◦ Infection control procedures? (ie, enteric precautions)
Dehydration
◦ Diarrhea and vomiting may lead to dehydration and electrolyte imbalance
◦ Encourage fluids during PT sessions
◦ Monitor BP and HR for volume depletion which can cause low BP and tachycardia
◦ Orthostatic hypotension
May need to stay close to toilet
◦ If patient able to participate in PT, ensure toilet nearby
◦ Don’t go commando!

constipation causes

◦ Bowel impaction
◦ Endocrine or neurogenic condition
◦ Sedentary lifestyle
◦ Poor diet (limited roughage, dehydration)
◦ Medications

constipation tx

◦ Surgery (reserved for impaction, structural issues, cancer)
◦ Nonsurgical:
◦ improved fiber and fluid supplementation
◦ increased physical activity
◦ pharmacologic treatmen

Bulk-Forming Laxatives MOA

increase water absorption = softens and increases bulk of intestinal contents

Bulk-Forming Laxatives effects

Distention of colon increases peristalsis
◦ Relatively safe, non-habit forming
◦ Not for individuals with abdominal pain, nausea, vomiting

Hyperosmotic Laxatives MOA

creates gradient that draws fluid into colon to increase stool fluid content and stimulate peristalsis

Hyperosmotic Laxatives AE

abdominal bloating, rectal irritation, electrolyte imbalance

Saline laxatives MOA

Similar to hyperosmotic– osmotic pressure pushes water/electrolytes into intestines

Saline laxatives AE

salts may cause issues with individual with diminished cardiac or renal function, electrolyte imbalance

Emollient Laxatives MOA

facilitate water and fat absorption into stool, lubricate fecal matter and intestinal wall

Emollient Laxatives AE

skin rash, decreased vitamin absorption, electrolyte imbalance
◦ Usually well-tolerated

Stimulant laxative MOA

stimulates peristalsis through enteric nervous system

Stimulant laxative AE

Danger of long-term use: dependence and damage to intestinal cells/loss of colon function

what are Known as fecal softeners and lubricant laxatives

emolient laxatives