Class 9: GI Flashcards
(175 cards)
1
Q
Types of acid-controlling drugs
A
Antacids, histamine-2 (H2) antagonists & proton pump inhibitors
2
Q
Acid-related pathophysiology
A
-The stomach secretes: HCl, bicarbonate, pepsinogen, intrinsic factor, mucus & prostaglandins (anti-inflammatory)
-Hyperacidity
3
Q
Antacids MOA
A
-Neutralize stomach acid
-Promote gastric mucosal defence mechanisms
4
Q
Antacids promote secretion of…
A
-Mucus; a protective barrier against HCl
-Bicarbonate; helps buffer HCl
-Prostaglandins; prevent activation of proton pump
5
Q
Antacids DO NOT…
A
Prevent the overproduction of acid
6
Q
Antacids DO..
A
Neutralize the acid once it is in the stomach
7
Q
Antacid effects
A
-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
8
Q
Antacids are used…
A
Alone or in combination with aluminum salts, magnesium salts, calcium salts or sodium bicarbonate
9
Q
Aluminum salts
A
-Almagel (with magnesium hydroxide)
-Combination products (aluminum and magnesium): Maalox, mylanta
10
Q
Magnesium salt
A
-Carbonate salt: Magmix
-Hydroxide salt: Milk of magnesia
-Oxide salt: Magnesium oxide
-Trisilicate salt: Gasulsol Tablets
-Combination product: Calmax, maalox
11
Q
Calcium salt are used to..
A
Prevent or treat calcium deficiency (calcium acetate, calcium liquid, and calcium carbonate (tums))
12
Q
Calcium salts are used in pt with
A
Kidney failure to bind dietary phosphate and reduce the amount of phosphorus absorbed from food
13
Q
Calcium salts used in pt with kidney failure include…
A
Aluminum hydroxide, calcium acetate, calcium carbonate, calcium liquid and sevelamer [Renagel]
14
Q
Sodium bicarbonate
A
-Is highly soluble
-Buffers the acidic properties of HCl
-Has a quick onset but short duration
15
Q
Sodium bicarbonate may cause..
A
-Metabolic alkalosis
-Problems in patients with HF, HTN, or renal insufficiency because of the high Na+ content
16
Q
Antacid contraindications
A
-Severe kidney failure or electrolyte disturbances (because of the potential toxic accumulation of electrolytes in the antacids themselves)
-GI obstruction
17
Q
Adverse effects of antacids
A
Minimal and depend on the compound used
18
Q
Aluminum & calcium adverse effects
A
Constipation
19
Q
Magnesium adverse effects
A
Diarrhea
20
Q
Calcium carbonate adverse effects
A
Produces gas and belching; combining it with simethicone reduces discomfort
21
Q
Antacid interactions + adsorption of other drugs
A
Adsorption of other drugs to antacids reduces the ability of the other drug to be absorbed into the body
22
Q
Antacid interactions + increased stomach pH
A
Increases the absorption of basic drugs & decreases the absorption of acidic drugs
23
Q
Antacid interactions + urinary pH
A
-Increased excretion of acidic drugs & decreased excretion of basic drugs
24
Q
Antacid nursing implications
A
-Assess for allergies and pre-existing conditions that may restrict the use of antacids, such as fluid imbalances, pregnancy & renal disease
25
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
26
Antacid adverse effects to monitor for...
-N/V, diarrhea & abdominal pain
-With calcium-containing products monitor for constipation, acid rebound
-Therapeutic response
27
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
28
Types of histamine-2 (H2) antagonists
-FNRC-H, "dines"
-Cimetidine
-Famotidine
-Nizatidine
-Ranitidine
29
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
30
H2 antagonist indications
GERD, PUD, erosive esophagitis, adjunct therapy in control of upper GI bleeding, and pathological gastric hypersecretory conditions
31
H2 antagonist adverse effects
-Very few adverse effects
-Cimetidine: Impotence & gynecomastia
-Headaches, lethargy, confusion, diarrhea, urticaria, sweating, flushing
32
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
33
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
34
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
35
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
36
To return to normal acid secretion following achlorhydria...
The parietal cell must synthesize new hydrogen–potassium–ATPase
37
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
38
Types of PPIs
-"prazoles" LORRPE
-Lansoprazole
-Omeprazole magnesium
-Rabeprazole & rabeprazole sodium
-Pantoprazole
-Esomeprazole
39
PPI drug effect safety & approval
-Safe for short-term therapy & adverse effects are uncommon
-Some approved for long-term therapy
40
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
41
PPI + diazepam or phenytoin
PPIs may increase serum levels of diazepam or phenytoin and cause increased chance for bleeding with warfarin (Coumadin)
42
PPIs work best when..
Taken 30-50 minutes before meals
43
Other antacids
Sucralfate, misoprostol & simethicone
44
Sucralfate
-A cytoprotective drug used for stress ulcers & PUD
45
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
46
Sucralfate adverse effects
Constipation, nausea & dry mouth
47
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
48
Sucralfate + phosphate
Binds with phosphate; may be used in chronic renal failure to reduce phosphate levels
49
Misoprostol
-A synthetic prostaglandin analogue
-Prostaglandins have cytoprotective functions
50
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
51
Misoprostol indications
Prevention of NSAID–induced gastric ulcers
52
Misoprostol dosing considerations
Doses that are therapeutic enough to treat duodenal ulcers often produce abdominal cramps, diarrhea
53
VC & CTZ
-Vomiting Centre (VC) & Chemoreceptor Trigger Zone (CTZ)
-Both are located in the brain and once stimulated, induce the vomiting reflex
54
Slide 36
55
Antiemetic drug MOA
Most work by blocking one of the vomiting pathways
56
Slide 38
57
Antiemetic drug indications
Prevention and reduction of N/V
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Antiemetic drug classes
-Anticholinergics, antihistamines, neuroleptics, prokinetics, serotonin blockers and tetrahydrocannabinol
59
Anticholinergics
Block ACh receptors in the vestibular nuclei & reticular formation
60
Antihistamines
Block H2 receptors thereby preventing ACh from binding to receptors in the vestibular nuclei
61
Neuroleptics
Block dopamine in the CTZ and may also block ACh
62
Prokinetics
Block dopamine in the CTZ or stimulate ACh receptors in the GI tract
63
Serotonin blockers
Block serotonin recepetors in the GI tract, CTZ & VC
64
Tetrahydrocannabinol
Have inhibitory effects on the reticular formation, thalamus & cerebral cortex
65
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
66
Anticholinergics include...
Scopolamine; used for motion sickness
67
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
68
Antihistamine (H1 receptor blocker) drugs
-DPMD
-Dimenhydrinate, diphenhydramine, meclizine & promethazine
69
MOA & other indications of neuroleptic drugs
-Block dopamine receptors on the CTZ
-Also used for psychotic disorders & intractable hiccups
70
Neuroleptic drugs
-CPP, "azines"
-Chlorpromazine, promethazine & perphenazine
71
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
72
Prokinetic drugs
Metoclopramide
73
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
74
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
75
Tetrahydrocannabinoids
Dronabinol & nabilone
76
Adverse effects of antiemetics
Stem from their nonselective blockade of various receptors
77
Slide 48
78
Nursing implications of antiemetics
-Can cause severe drowsiness
-Can cause CNS depression when taken with alcohol
-Change positions slowly to avoid orthostatic hypotension
79
Antiemetic nursing implications cont'd
Given 1 to 3 hours before a chemotherapy drug
80
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
81
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
82
Acute diarrhea
-Occurs suddenly in a previously healthy person
-Lasts from 3 days to 2 weeks
Is self-limiting
-Resolves without sequelae
83
Categories of antidiarrheals
Probiotics & intestinal flora modifiers, adsorbents, anticholinergics and opiates
84
Adsorbents
Activated charcoal, aluminum hydroxide, bismuth subsalicylate, cholestyramine & polycarbophil
85
Anticholinergics
Atropine sulphate & hyoscyamine
86
Opiates
Opium tincture, paregoric, codeine phosphate, diphenoxylate & kepramide hydrochloride
87
Probiotics & intestinal flora modifiers
Lactobacillus acidophillus, lactobacillus GG & saccharomyces boulardii
88
Adsorbents MOA
-Coat the walls of the gastrointestinal (GI) tract
-Bind to the causative bacteria or toxin, which is then eliminated through the stool
89
Types of adsorbents
Bismuth subsalicylate, activated charcoal & attapulgite
90
Anticholinergic MOA
-Decrease intestinal muscle tone and peristalsis of GI tract
-Slow the movement of fecal matter through the GI tract
91
Anticholinergic drug types
Belladonna alkaloids, atropine, hyoscyamine & hyoscine
92
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
93
Antimotility drugs: Opiate drugs
Paregoric, opium tincture, codeine, loperamide & diphenoxylate
94
Antidiarrheals: Intestinal flora modifiers
-Are also known as probiotics or bacterial replacement drugs
-Are bacterial cultures of Lactobacillus organisms
-Includes L. acidophilus
95
Lactobacillus organisms work by...
-Supplying missing bacteria to the GI tract
-Suppressing the growth of diarrhea-causing bacteria
96
Antidiarrheal combination products
Diphenoxylate with subtherapeutic amounts of atropine which discourages recreational opiate drug use
97
Large doses of diphenoxylate & atropine result in...
Extreme anticholinergic effects such as dry mouth, blurred vision, abdominal pain & tachycardia
98
Adverse effects of antidiarrheal adsorbents
-Increased bleeding time, constipation, dark stools, confusion & twitching
-Hearing loss, tinnitus, metallic taste & blue gums
99
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
100
Adverse effects of antidirrheal opiates
-Drowsiness, dizziness, sedation, lethargy, N/V, anorexia & constipation
-Respiratory depression, bradycardia, palpitations & hypotension
-Urinary retention, flushing, rash, urticaria
101
Antidiarrheal adsorbent interactions
-Adsorbents decrease the absorption of digoxin, clindamycin, quinidine & hypoglycemic drugs
-Adsorbents cause increased bleeding time and bruising when given with anticoagulants
102
Antacids + anticholinergic antidiarrheals
Antacids can decrease the effects of anticholinergic antidiarrheal drugs
103
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
104
Antidiarrheal administration considerations
Assess fluid volume status, intake & output, and mucous membranes before, during, and after treatment
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Slide 65
106
Bulk forming laxatives
Psyllium, methylcellulose & polycarbophil
107
Emolient laxatives
Docusate sodium & mineral oil
108
Hyperosmotic laxatives
Polyethylene glycol (PEG), lactulose, sorbitol & glycerin
109
Saline laxatives
Magnesium sulphate, magnesium citrate, magnesium hydroxide, magnesium phosphate & sodium phosphate
110
Stimulant laxatives
Senna, biscodyl, cascara sagrada & castor oil
111
Bulk forming laxative MOA
High in fibre, absorb water to increase bulk and distend bowel to initiate reflex bowel activity
112
Emolient laxative MOA
-AKA stool softeners and lubricants
-Promote more water and fat in the stools, lubricate fecal material & intestinal walls
113
Hyperosmotic laxative MOA
-Increase fecal water content resulting in bowel distention, increased peristalsis & evacuation
-Used for diagnostic & surgical preparation
114
Lactulose liquid is also used to..
Reduce elevated serum ammonia levels
115
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
116
Stimulant laxative MOA
Increase peristalsis via intestinal nerve stimulation
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All laxatives
-Increase peristalsis and water & focal mass
-Softens fecal mass
118
All laxatives increasesecretion of water & electolytes in the small bowel except..
Hyperosmotics
119
All laxatives inhibit absorption of water in the small bowel except...
Hyperosmotics
120
All laxatives increase wall permeability in the small bowel except...
Hyperosmotics & saline
121
All laxatives act only in the large bowel except...
Saline & stimulants
122
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
123
All laxatives can cause..
Electrolyte imbalances
124
Bulk forming laxative adverse effects
Impaction, fluid overload & esophageal blockage
125
Emolient laxative adverse effects
Skin rashes & decreased absorption of vitamins
126
Hyperosmotic adverse effects
Abdominal bloating & rectal irritation
127
Saline laxative adverse effects
Magnesium toxicity (with renal insufficiency), cramping, diarrhea & increased thirst
128
Stimulant laxative adverse effects
Nutrient malabsorption, skin rashes, rectal & gastric irritation
129
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
130
Patients should not take a laxative or cathartic if they are...
Experiencing N/V or abdominal pain
131
Assessments before administering a laxative
Assess fluid and electrolytes before initiating therapy
132
Take laxative tablets with...
180 to 240mL of water
133
Take bulk forming laxatives with...
240mL of water
134
Alternatives to laxatives..
A high-fibre diet and increased fluid intake is preferred to laxative use
135
Long-term laxative use often...
Results in decreased bowel tone and may lead to dependency
136
All laxative tablets should be...
Swallowed whole, not crushed or chewed, especially if enteric coated
137
Bisocodyl & cascara sagrada should be...
Given with water due to interactions with milk, antacids and juices
138
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
139
Disorders of the stomach & upper small intestine
GERD, acute gastritis, upper GI bleed & PUD
140
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
141
Upper GI bleed collaborative care
Endoscopic, surgical & drug therapy
142
Upper GI bleed nursing implementations
Health promotion, acute intervention & ambulatory and home care
143
PUD drug therapy
H2‑receptor blockers, PPIs, antibiotics, antacids, anticholinergics & cytoprotective drug therapy
144
PUD nursing implementation
-Health promotion
-Acute intervention of: Hemorrhaging, perforation & gastric outlet obstruction
-Ambulatory and home care
145
PUD postoperative complications
Dumping syndrome, postprandial hypoglycemia & bile reflux gastritis
146
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
147
Acute abdominal pain acute interventions
Preoperative & postoperative care
148
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
149
Types of intestinal obstruction
Mechanical & nonmechanical
150
Slide 94
151
Disorders of the liver
Viral hepatitis, toxic and drug-induced hepatitis, nonalcoholic fatty liver disease and nonalcoholic steatohepatitis
152
Hepatitis drug therapy goals
-Decrease viral load & liver enzyme levels
-Decrease rate of disease progression: a-interferon, nucleoside and nucleutide analogs
153
Acute intervention of hepatitis
Jaundice & rest
154
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
155
Hepatic steatosis
Accumulation of fat in the liver
156
Diagnositic studies of liver cirrhosis
Liver biopsy & noninvasive fibrosis markers
157
Collaborative care of liver cirrhosis
-Drug therapy
-Ascites may require a peritoneovenous shunt
158
Acute intervention of liver cirrhosis
-Ruptured esophageal varices
-Hepatic encephalopathy
159
Collaborative care of acute pancreatitis
Conservative, surgical, drug & nutritional therapy
160
Etiology of bleeding tendencies
Lack of or decreased absorption of vitamin K resulting in decreased production of prothrombin
161
Etiology of clay-coloured stools
Blockage of flow of bile salts out of the liver
162
Etiology of dark amber urine that foams when shaken
Soluble bilirubin in the urine
163
Etiology of intolerance to fatty foods (nausea, sensation of fullness & anorexia)
No bile in the small intestine for fat absorption
164
Etiology of no urobilinogen in the urine
No bilirubin reaching the small intestine to be converted to uroglobilinogen
165
Etiology of obstructive jaundice
No bile flow into the duodenum
166
Etiology of pruritis
Deposition of bile salts in the skin tissues
167
Etiology of steatorrhea
No bile salts in the duodenum preventing fat emulsion & digestion
168
Collaborative care of cholethiases & cholesystitis
Conservative, surgical, transhepatic biliary catheter, drug & nutritional therapy
169
Cholecystectomy
Removal of the gallbladder
170
Cholecystostomy (usually an emergency procedure)
Incision into gallbladder (usually for the removal of gallstones)
171
Choledocholithotomy
Incision into the common bile duct for removal of stones
172
Cholescystogastrostomy
Anastomosis between the stomach & gallbladder
173
Cholecystoduodenostomy
Anastomosis between the gallbladder & duodenum to relieve obstruction at the distal end of the common bile duct
174
Laproscopic cholecystectomy
Removal of the gallbladder via laparoscopy through the use of a dissecting laser
175
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
