Class 9: GI Flashcards
Types of acid-controlling drugs
Antacids, histamine-2 (H2) antagonists & proton pump inhibitors
Acid-related pathophysiology
-The stomach secretes: HCl, bicarbonate, pepsinogen, intrinsic factor, mucus & prostaglandins (anti-inflammatory)
-Hyperacidity
Antacids MOA
-Neutralize stomach acid
-Promote gastric mucosal defence mechanisms
Antacids promote secretion of…
-Mucus; a protective barrier against HCl
-Bicarbonate; helps buffer HCl
-Prostaglandins; prevent activation of proton pump
Antacids DO NOT…
Prevent the overproduction of acid
Antacids DO..
Neutralize the acid once it is in the stomach
Antacid effects
-Reduce acid associated pain
-Raising gastric pH by 0.3 neutralizes 50% of the gastric acid
-Raising gastric pH one point neutralizes 90% of the gastric acid
Antacids are used…
Alone or in combination with aluminum salts, magnesium salts, calcium salts or sodium bicarbonate
Aluminum salts
-Almagel (with magnesium hydroxide)
-Combination products (aluminum and magnesium): Maalox, mylanta
Magnesium salt
-Carbonate salt: Magmix
-Hydroxide salt: Milk of magnesia
-Oxide salt: Magnesium oxide
-Trisilicate salt: Gasulsol Tablets
-Combination product: Calmax, maalox
Calcium salt are used to..
Prevent or treat calcium deficiency (calcium acetate, calcium liquid, and calcium carbonate (tums))
Calcium salts are used in pt with
Kidney failure to bind dietary phosphate and reduce the amount of phosphorus absorbed from food
Calcium salts used in pt with kidney failure include…
Aluminum hydroxide, calcium acetate, calcium carbonate, calcium liquid and sevelamer [Renagel]
Sodium bicarbonate
-Is highly soluble
-Buffers the acidic properties of HCl
-Has a quick onset but short duration
Sodium bicarbonate may cause..
-Metabolic alkalosis
-Problems in patients with HF, HTN, or renal insufficiency because of the high Na+ content
Antacid contraindications
-Severe kidney failure or electrolyte disturbances (because of the potential toxic accumulation of electrolytes in the antacids themselves)
-GI obstruction
Adverse effects of antacids
Minimal and depend on the compound used
Aluminum & calcium adverse effects
Constipation
Magnesium adverse effects
Diarrhea
Calcium carbonate adverse effects
Produces gas and belching; combining it with simethicone reduces discomfort
Antacid interactions + adsorption of other drugs
Adsorption of other drugs to antacids reduces the ability of the other drug to be absorbed into the body
Antacid interactions + increased stomach pH
Increases the absorption of basic drugs & decreases the absorption of acidic drugs
Antacid interactions + urinary pH
-Increased excretion of acidic drugs & decreased excretion of basic drugs
Antacid nursing implications
-Assess for allergies and pre-existing conditions that may restrict the use of antacids, such as fluid imbalances, pregnancy & renal disease
Antacid nursing implications cont’d
-Many drug interactions; most drugs should be given 1 to 2 hours after giving an antacid
-Antacids may cause premature dissolving of enteric-coated medications resulting in stomach upset
Antacid adverse effects to monitor for…
-N/V, diarrhea & abdominal pain
-With calcium-containing products monitor for constipation, acid rebound
-Therapeutic response
About histamine-2 (H2) antagonists
-Reduce acid secretion
-Are available OTC in lower dosage forms
-The most popular drugs for treatment of acid-related disorders
Types of histamine-2 (H2) antagonists
-FNRC-H, “dines”
-Cimetidine
-Famotidine
-Nizatidine
-Ranitidine
Histamine-2 (H2) antagonist MOA
-Block histamine at the H2 receptors of acid-producing parietal cells
-Reduce production of hydrogen ions, resulting in decreased production of HCl
-Suppresses secretion of stomach acid
H2 antagonist indications
GERD, PUD, erosive esophagitis, adjunct therapy in control of upper GI bleeding, and pathological gastric hypersecretory conditions
H2 antagonist adverse effects
-Very few adverse effects
-Cimetidine: Impotence & gynecomastia
-Headaches, lethargy, confusion, diarrhea, urticaria, sweating, flushing
H2 antagonist interactions
-Cimetidine binds with P-450 microsomal oxidase system in the liver and inhibits oxidation of many drugs and increases drug levels
-Inhibits absorption of drugs that require an acidic environment for absorption
-Smoking decreases the effectiveness of H2 blockers
Nursing implications of H2 antagonists
-Assess for allergies and impaired renal or liver function
-Use with caution in patients who are confused and in older adults
-Give 1 hour before or after antacids
Proton pump
-Parietal cells release +hydrogen ions (protons) during HCl production
-This process is called the “proton pump”
-H2 blockers & antihistamines do not stop the action of the pump
Proton Pump Inhibitors (PPIs)
-Irreversibly bind to the hydrogen–potassium–ATPase enzyme preventing the movement of hydrogen ions
-Results in achlorhydria; blockage of gastric acid secretion
To return to normal acid secretion following achlorhydria…
The parietal cell must synthesize new hydrogen–potassium–ATPase
PPI drug effect
-Total inhibition of gastric acid secretion
-GERD maintenance therapy
-Short-term tx of active duodenal & gastric ulcers
-Tx of H. pylori induced ulcers, given with an antibiotic
-Tx of Zollinger-Ellison syndrome
Types of PPIs
-“prazoles” LORRPE
-Lansoprazole
-Omeprazole magnesium
-Rabeprazole & rabeprazole sodium
-Pantoprazole
-Esomeprazole
PPI drug effect safety & approval
-Safe for short-term therapy & adverse effects are uncommon
-Some approved for long-term therapy
PPI nursing implications + pantoprazole
-Pantoprazole is the only proton pump inhibitor available for parenteral administration and can be used in pt that are unable to take PO medications
PPI + diazepam or phenytoin
PPIs may increase serum levels of diazepam or phenytoin and cause increased chance for bleeding with warfarin (Coumadin)
PPIs work best when..
Taken 30-50 minutes before meals
Other antacids
Sucralfate, misoprostol & simethicone
Sucralfate
-A cytoprotective drug used for stress ulcers & PUD
Sucralfate MOA
-Binds to the base of ulcers & erosions forming a protective barrier
-Protects these areas from pepsin which normally breaks down proteins and makes ulcers worse
-Absorbs little from the gut
Sucralfate adverse effects
Constipation, nausea & dry mouth
Sucralfate nursing interactions
-May impair absorption of other drugs—give other drugs at least 2 hours before giving sucralfate
-Should not be administered with other medications
Sucralfate + phosphate
Binds with phosphate; may be used in chronic renal failure to reduce phosphate levels
Misoprostol
-A synthetic prostaglandin analogue
-Prostaglandins have cytoprotective functions
Prostaglandin cytoprotetive functions
-Protect gastric mucosa from injury by enhancing local production of mucus or bicarbonate
-Promote local cell regeneration & help to maintain mucosal blood flow
Misoprostol indications
Prevention of NSAID–induced gastric ulcers
Misoprostol dosing considerations
Doses that are therapeutic enough to treat duodenal ulcers often produce abdominal cramps, diarrhea
VC & CTZ
-Vomiting Centre (VC) & Chemoreceptor Trigger Zone (CTZ)
-Both are located in the brain and once stimulated, induce the vomiting reflex
Slide 36
Antiemetic drug MOA
Most work by blocking one of the vomiting pathways
Slide 38
Antiemetic drug indications
Prevention and reduction of N/V
Antiemetic drug classes
-Anticholinergics, antihistamines, neuroleptics, prokinetics, serotonin blockers and tetrahydrocannabinol
Anticholinergics
Block ACh receptors in the vestibular nuclei & reticular formation
Antihistamines
Block H2 receptors thereby preventing ACh from binding to receptors in the vestibular nuclei
Neuroleptics
Block dopamine in the CTZ and may also block ACh
Prokinetics
Block dopamine in the CTZ or stimulate ACh receptors in the GI tract
Serotonin blockers
Block serotonin recepetors in the GI tract, CTZ & VC
Tetrahydrocannabinol
Have inhibitory effects on the reticular formation, thalamus & cerebral cortex
Anticholinergics (ACh blockers): Other indications
-Bind to and block acetylcholine (ACh) receptors in the inner ear labyrinth
-Block transmission of nauseating stimuli to CTZ & from the reticular formation to the VC
Anticholinergics include…
Scopolamine; used for motion sickness
MOA & other indications of antihistamine drugs
-Inhibit ACh by binding to H1 receptors
-Prevent cholinergic stimulation in vestibular and reticular areas, thus preventing N/V
-Also used for motion sickness, nonproductive cough, allergy symptoms & sedation
Antihistamine (H1 receptor blocker) drugs
-DPMD
-Dimenhydrinate, diphenhydramine, meclizine & promethazine
MOA & other indications of neuroleptic drugs
-Block dopamine receptors on the CTZ
-Also used for psychotic disorders & intractable hiccups
Neuroleptic drugs
-CPP, “azines”
-Chlorpromazine, promethazine & perphenazine
MOA & other indications of prokinetic drugs
-Block dopamine in the CTZ
-Desensitize CTZ to impulses it receives from the GI tract
-Stimulate peristalsis in GI tract, enhancing emptying of stomach contents
-Can also be used for used for GERD & delayed gastric emptying
Prokinetic drugs
Metoclopramide
MOA & other indications of serotonin blockers
-Block serotonin receptors in the GI tract, CTZ, and VC
-Used for N/V in patients receiving chemotherapy and in the postoperative period
MOA & other indications of tetrahydrocannabinoids (THC)
-Alter mood and body’s perception of its surroundings
-Used for N/V associated with chemotherapy & anorexia associated with weight loss in patients with AIDS
Tetrahydrocannabinoids
Dronabinol & nabilone
Adverse effects of antiemetics
Stem from their nonselective blockade of various receptors
Slide 48
Nursing implications of antiemetics
-Can cause severe drowsiness
-Can cause CNS depression when taken with alcohol
-Change positions slowly to avoid orthostatic hypotension
Antiemetic nursing implications cont’d
Given 1 to 3 hours before a chemotherapy drug
Age-related considerations of N/V
Older adult patients experiencing nausea and vomiting require careful assessment and monitoring, particularly during periods of fluid loss and subsequent rehydration therapy
Age-related considerations of N/V cont’d
-They are more likely to have cardiac or renal insufficiency that places them at greater risk for life-threatening fluid & electrolyte imbalances
-Excessive replacement of fluid & electrolytes may result in adverse consequences in older adults with HF or renal disease
Acute diarrhea
-Occurs suddenly in a previously healthy person
-Lasts from 3 days to 2 weeks
Is self-limiting
-Resolves without sequelae
Categories of antidiarrheals
Probiotics & intestinal flora modifiers, adsorbents, anticholinergics and opiates
Adsorbents
Activated charcoal, aluminum hydroxide, bismuth subsalicylate, cholestyramine & polycarbophil
Anticholinergics
Atropine sulphate & hyoscyamine
Opiates
Opium tincture, paregoric, codeine phosphate, diphenoxylate & kepramide hydrochloride
Probiotics & intestinal flora modifiers
Lactobacillus acidophillus, lactobacillus GG & saccharomyces boulardii
Adsorbents MOA
-Coat the walls of the gastrointestinal (GI) tract
-Bind to the causative bacteria or toxin, which is then eliminated through the stool
Types of adsorbents
Bismuth subsalicylate, activated charcoal & attapulgite
Anticholinergic MOA
-Decrease intestinal muscle tone and peristalsis of GI tract
-Slow the movement of fecal matter through the GI tract
Anticholinergic drug types
Belladonna alkaloids, atropine, hyoscyamine & hyoscine
Antimotility drugs: Opiates MOA
-Decrease bowel motility and relieve rectal spasms (reduces pain)
-Decrease transit time through the bowel, allowing more time for water and electrolytes to be absorbed
Antimotility drugs: Opiate drugs
Paregoric, opium tincture, codeine, loperamide & diphenoxylate
Antidiarrheals: Intestinal flora modifiers
-Are also known as probiotics or bacterial replacement drugs
-Are bacterial cultures of Lactobacillus organisms
-Includes L. acidophilus
Lactobacillus organisms work by…
-Supplying missing bacteria to the GI tract
-Suppressing the growth of diarrhea-causing bacteria
Antidiarrheal combination products
Diphenoxylate with subtherapeutic amounts of atropine which discourages recreational opiate drug use
Large doses of diphenoxylate & atropine result in…
Extreme anticholinergic effects such as dry mouth, blurred vision, abdominal pain & tachycardia
Adverse effects of antidiarrheal adsorbents
-Increased bleeding time, constipation, dark stools, confusion & twitching
-Hearing loss, tinnitus, metallic taste & blue gums
Adverse effects of antidiarrheal anticholinergics
-Urinary retention, hesitance & impotence
-Headache, dizziness, confusion, anxiety & drowsiness
-Dry skin, rash & flushing
-Blurred vision, photophobia & increased intraocular pressure
-Hypotension, HTN, bradycardia & tachycardia
Adverse effects of antidirrheal opiates
-Drowsiness, dizziness, sedation, lethargy, N/V, anorexia & constipation
-Respiratory depression, bradycardia, palpitations & hypotension
-Urinary retention, flushing, rash, urticaria
Antidiarrheal adsorbent interactions
-Adsorbents decrease the absorption of digoxin, clindamycin, quinidine & hypoglycemic drugs
-Adsorbents cause increased bleeding time and bruising when given with anticoagulants
Antacids + anticholinergic antidiarrheals
Antacids can decrease the effects of anticholinergic antidiarrheal drugs
Antidiarrheal nursing considerations
-Do NOT give bismuth subsalicylate (Pepto-Bismol) to children or teenagers with chickenpox because of the risk of Reye’s syndrome
-Teach patients to take medications exactly as prescribed and to be aware of their fluid intake and dietary changes
Antidiarrheal administration considerations
Assess fluid volume status, intake & output, and mucous membranes before, during, and after treatment
Slide 65
Bulk forming laxatives
Psyllium, methylcellulose & polycarbophil
Emolient laxatives
Docusate sodium & mineral oil
Hyperosmotic laxatives
Polyethylene glycol (PEG), lactulose, sorbitol & glycerin
Saline laxatives
Magnesium sulphate, magnesium citrate, magnesium hydroxide, magnesium phosphate & sodium phosphate
Stimulant laxatives
Senna, biscodyl, cascara sagrada & castor oil
Bulk forming laxative MOA
High in fibre, absorb water to increase bulk and distend bowel to initiate reflex bowel activity
Emolient laxative MOA
-AKA stool softeners and lubricants
-Promote more water and fat in the stools, lubricate fecal material & intestinal walls
Hyperosmotic laxative MOA
-Increase fecal water content resulting in bowel distention, increased peristalsis & evacuation
-Used for diagnostic & surgical preparation
Lactulose liquid is also used to..
Reduce elevated serum ammonia levels
Saline laxative MOA + use
-Increase osmotic pressure within the intestinal tract, causing more water to enter the intestines
-Results in bowel distention, increased peristalsis & evacuation
-Used for diagnostic and surgical prep and removal of helminths and parasites
Stimulant laxative MOA
Increase peristalsis via intestinal nerve stimulation
All laxatives
-Increase peristalsis and water & focal mass
-Softens fecal mass
All laxatives increasesecretion of water & electolytes in the small bowel except..
Hyperosmotics
All laxatives inhibit absorption of water in the small bowel except…
Hyperosmotics
All laxatives increase wall permeability in the small bowel except…
Hyperosmotics & saline
All laxatives act only in the large bowel except…
Saline & stimulants
Laxative contraindications
-Use with caution with:
-Acute surgical abdomen, appendicitis symptoms such as N/V and fecal impaction (mineral oil enemas excepted)
-Intestinal obstruction & undiagnosed abdominal pain
All laxatives can cause..
Electrolyte imbalances
Bulk forming laxative adverse effects
Impaction, fluid overload & esophageal blockage
Emolient laxative adverse effects
Skin rashes & decreased absorption of vitamins
Hyperosmotic adverse effects
Abdominal bloating & rectal irritation
Saline laxative adverse effects
Magnesium toxicity (with renal insufficiency), cramping, diarrhea & increased thirst
Stimulant laxative adverse effects
Nutrient malabsorption, skin rashes, rectal & gastric irritation
Laxative interactions
-Because laxatives alter intestinal function they can interact with other drugs quite readily
-Each category can alter the effect of specific drugs
-Some laxatives may interact with food such as milk and juices
Patients should not take a laxative or cathartic if they are…
Experiencing N/V or abdominal pain
Assessments before administering a laxative
Assess fluid and electrolytes before initiating therapy
Take laxative tablets with…
180 to 240mL of water
Take bulk forming laxatives with…
240mL of water
Alternatives to laxatives..
A high-fibre diet and increased fluid intake is preferred to laxative use
Long-term laxative use often…
Results in decreased bowel tone and may lead to dependency
All laxative tablets should be…
Swallowed whole, not crushed or chewed, especially if enteric coated
Bisocodyl & cascara sagrada should be…
Given with water due to interactions with milk, antacids and juices
Contact physician if a pt experiences blank when taking laxatives
Severe abdominal pain, muscle weakness, cramps, or dizziness which may indicate possible fluid or electrolyte loss
Disorders of the stomach & upper small intestine
GERD, acute gastritis, upper GI bleed & PUD
GERD pt teaching
Smoking cessation, elevate head of bed 30 degrees, avoid lying down for 2 to 3 hours after eating and avoid late-night eating
Upper GI bleed collaborative care
Endoscopic, surgical & drug therapy
Upper GI bleed nursing implementations
Health promotion, acute intervention & ambulatory and home care
PUD drug therapy
H2‑receptor blockers, PPIs, antibiotics, antacids, anticholinergics & cytoprotective drug therapy
PUD nursing implementation
-Health promotion
-Acute intervention of: Hemorrhaging, perforation & gastric outlet obstruction
-Ambulatory and home care
PUD postoperative complications
Dumping syndrome, postprandial hypoglycemia & bile reflux gastritis
Age related considerations with PUD
-Recent increased incidence in >60 years of age d/t the use of NSAIDS
-Pain may not be the first symptom, look for frank gastric bleeding (hematemesis/melena) or a decreased hematocrit
-Higher morbidity/mortality rates d/t comborbidities & decreased ability to withstand hypovolemia
Acute abdominal pain acute interventions
Preoperative & postoperative care
Abdominal trauma emergency management
-Focuses on establishing an airway & adequate breathing, fluid replacement, and prevention of hypovolemic shock
-Establish IV access and administer volume expanders or blood if the pt is hypotensive
Types of intestinal obstruction
Mechanical & nonmechanical
Slide 94
Disorders of the liver
Viral hepatitis, toxic and drug-induced hepatitis, nonalcoholic fatty liver disease and nonalcoholic steatohepatitis
Hepatitis drug therapy goals
-Decrease viral load & liver enzyme levels
-Decrease rate of disease progression: a-interferon, nucleoside and nucleutide analogs
Acute intervention of hepatitis
Jaundice & rest
Nonalcoholic fatty liver disease (NAFLD)
-A spectrum of disease that ranges from simple fatty liver that causes no hepatic inflammation to severe liver scarring
-Characterized by hepatic steatosis associated with other causes
Hepatic steatosis
Accumulation of fat in the liver
Diagnositic studies of liver cirrhosis
Liver biopsy & noninvasive fibrosis markers
Collaborative care of liver cirrhosis
-Drug therapy
-Ascites may require a peritoneovenous shunt
Acute intervention of liver cirrhosis
-Ruptured esophageal varices
-Hepatic encephalopathy
Collaborative care of acute pancreatitis
Conservative, surgical, drug & nutritional therapy
Etiology of bleeding tendencies
Lack of or decreased absorption of vitamin K resulting in decreased production of prothrombin
Etiology of clay-coloured stools
Blockage of flow of bile salts out of the liver
Etiology of dark amber urine that foams when shaken
Soluble bilirubin in the urine
Etiology of intolerance to fatty foods (nausea, sensation of fullness & anorexia)
No bile in the small intestine for fat absorption
Etiology of no urobilinogen in the urine
No bilirubin reaching the small intestine to be converted to uroglobilinogen
Etiology of obstructive jaundice
No bile flow into the duodenum
Etiology of pruritis
Deposition of bile salts in the skin tissues
Etiology of steatorrhea
No bile salts in the duodenum preventing fat emulsion & digestion
Collaborative care of cholethiases & cholesystitis
Conservative, surgical, transhepatic biliary catheter, drug & nutritional therapy
Cholecystectomy
Removal of the gallbladder
Cholecystostomy (usually an emergency procedure)
Incision into gallbladder (usually for the removal of gallstones)
Choledocholithotomy
Incision into the common bile duct for removal of stones
Cholescystogastrostomy
Anastomosis between the stomach & gallbladder
Cholecystoduodenostomy
Anastomosis between the gallbladder & duodenum to relieve obstruction at the distal end of the common bile duct
Laproscopic cholecystectomy
Removal of the gallbladder via laparoscopy through the use of a dissecting laser
Laparoscopic cholecystectomy postoperative care
-Remove bandages the day after surgury, bathe or shower
-Notify the surgeon of any redness, swelling, bile-coloured drainage or pus, severe abdominal pain, N/V, fever & chills
-AAT, return to work within 1 week
-DAT, low-fat is typically tolerated better
